Статті в журналах: "Distal suppressor"

1

Maine, E. M., and J. Kimble. "Suppressors of glp-1, a gene required for cell communication during development in Caenorhabditis elegans, define a set of interacting genes." Genetics 135, no. 4 (December 1, 1993): 1011–22. http://dx.doi.org/10.1093/genetics/135.4.1011.

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Abstract The glp-1 gene is essential for two cell interactions that control cell fate in Caenorhabditis elegans: induction of anterior pharynx in the embryo and induction of mitotic proliferation in the germ line. To identify other genes involved in these cell interactions, we have isolated suppressors of two temperature sensitive alleles of glp-1. Each of 14 recessive suppressors rescues both embryonic and germline glp-1(ts) defects. These suppressors are extragenic and define a set of six genes designated sog, for suppressor of glp-1. Suppression of glp-1 is the only obvious phenotype associated with sog mutations. Mutations in different sog genes show allele-specific intergenic noncomplementation, suggesting that the sog gene products may interact. In addition, we have analyzed a semidominant mutation that suppresses only the glp-1 germline phenotype and has a conditional feminized phenotype of its own. None of the suppressors rescues a glp-1 null mutation and therefore they do not bypass a requirement for glp-1. Distal tip cell function remains necessary for germline proliferation in suppressed animals. These suppressor mutations identify genes that may encode other components of the glp-1 mediated cell-signaling pathway or regulate glp-1 expression.

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2

Haverkamp., Jessica, and Timothy Ratliff. "Regulatory function of myeloid-derived suppressor cells is restricted to inflammatory site. (98.25)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 98.25. http://dx.doi.org/10.4049/jimmunol.184.supp.98.25.

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Abstract Myeloid-derived suppressor cells (MDSC) are identified in mice as Gr-1+CD11b+ cells able to suppress T cell proliferation. Suppressive function of MDSC is linked to expression of arginase I and inducible nitric oxide synthase (iNOS) and can be augmented by inflammation. While inflammation is linked to MDSC function, it is unknown if MDSC isolated from the inflammatory site possess equal regulatory function as those in distal sites such as the spleen. Using the POET-3 model of prostate inflammation, we show Gr-1+CD11b+ cells isolated from inflamed prostates express elevated levels of ARG I and iNOS. In contrast, cells from the spleens of mice with prostate inflammation do not express detectable levels of ARG I or iNOS. However, when function of Gr-1+CD11b+ cells from spleens or the inflammatory site were tested in conventional suppression assays, all cells demonstrated suppressive function. RT-PCR analysis revealed that arginase I and iNOS mRNA were induced in MDSC during suppression assays, in part through IFN-γ. Thus conventional suppression assays induce functional suppressor cells and do not test their actual activation state in vivo. To better evaluate the function of Gr-1+CD11b+ cells we developed a short term suppression assay designed to limit exposure to IFN-γ during culture. Only cells from the inflammatory site suppressed T cell proliferation. These data demonstrate the novel finding that only Gr-1+CD11b+ cells at the inflammatory site are functional MDSC.

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3

Käfer, Etta. "MMS Sensitivity of All Amino Acid-Requiring Mutants in Aspergillus and Its Suppression by Mutations in a Single Gene." Genetics 115, no. 4 (April 1, 1987): 671–76. http://dx.doi.org/10.1093/genetics/115.4.671.

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ABSTRACT All available amino acid-requiring mutants of Aspergillus nidulans were found to be hypersensitive to MMS (methyl methanesulfonate) to various degrees. On MMS media, secondary mutations could be selected which suppress this MMS sensitivity but do not affect the requirement. Many such mutations were analyzed and found to be alleles of one gene, smsA (=suppressor of MMS sensitivity), which mapped distal on the right arm of chromosome V. This gene is more likely to be involved in general regulation of amino acid biosynthesis than MMS uptake, since a variety of pathway interactions were clearly modified by smsA suppressors in the absence of MMS.

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4

Hollingsworth, N. M., and A. D. Johnson. "A conditional allele of the Saccharomyces cerevisiae HOP1 gene is suppressed by overexpression of two other meiosis-specific genes: RED1 and REC104." Genetics 133, no. 4 (April 1, 1993): 785–97. http://dx.doi.org/10.1093/genetics/133.4.785.

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Abstract The HOP1 gene of Saccharomyces cerevisiae is believed to encode a protein component of the synaptonemal complex, the structure formed when homologous chromosomes synapse during meiotic prophase. Five new mutant alleles (three conditional, two nonconditional) of HOP1 were identified by screening EMS-mutagenized cells for a failure to complement the spore viability defect of a hop1 null allele. Two high copy plasmids were found that partially suppress the temperature-sensitive spore inviability phenotype of one of these alleles, hop1-628. The suppression is allele-specific; no effect of the plasmids is observed in hop1 null diploids. Mutation of either of the two suppressor genes results in recessive spore lethality, indicating that these genes play important roles during meiosis. The DNA sequence of one high copy suppressor gene matched that of RED1, a previously identified meiosis-specific gene. Our data strongly support the idea that RED1 protein is also a component of the synaptonemal complex and further suggest that the RED1 and HOP1 gene products may interact. The second suppressor maps to the right arm of chromosome VIII distal to CDC12 and is REC104, a meiosis-specific gene believed to act early in meiosis.

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5

Strand, D. J., and J. F. McDonald. "Insertion of a copia element 5' to the Drosophila melanogaster alcohol dehydrogenase gene (adh) is associated with altered developmental and tissue-specific patterns of expression." Genetics 121, no. 4 (April 1, 1989): 787–94. http://dx.doi.org/10.1093/genetics/121.4.787.

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Abstract The Drosophila melanogaster alcohol dehydrogenase gene (adh) is under the control of two separate promoters (proximal and distal) which are preferentially utilized at the larval and adult life stages, respectively. A variant alcohol dehydrogenase allele (RI-42) isolated from a natural population contains a copia retroviral-like transposable element inserted 240 bp upstream from the distal (adult) adh transcriptional start site. Levels of adh transcripts in the RI-42 variant are reduced in tissues and at life stages where copia is actively expressed and are affected in trans- by mutant alleles at the suppressor-of-white-apricot (su(wa] and suppressor-of-forked (su(f] loci. These suppressor genes have no effect on adh expression in wild-type Drosophila.

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6

Lissemore, J. L., P. D. Currie, C. M. Turk, and E. M. Maine. "Intragenic dominant suppressors of glp-1, a gene essential for cell-signaling in Caenorhabditis elegans, support a role for cdc10/SWI6/ankyrin motifs in GLP-1 function." Genetics 135, no. 4 (December 1, 1993): 1023–34. http://dx.doi.org/10.1093/genetics/135.4.1023.

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Abstract The glp-1 gene product mediates cell-cell interactions required for cell fate specification during development in Caenorhabditis elegans. To identify genes that interact with glp-1, we screened for dominant suppressors of two temperature-sensitive glp-1 alleles and recovered 18 mutations that suppress both germline and embryonic glp-1 phenotypes. These dominant suppressors are tightly linked to glp-1 and do not bypass the requirement for a distal tip cell, which is thought to be the source of a signal that is received and transduced by the GLP-1 protein. Using single-strand conformation polymorphism (SSCP) analysis and DNA sequencing, we found that at least 17 suppressors are second-site intragenic revertants. The suppressors, like the original glp-1(ts) mutations, are all located in the cdc10/SWI6/ankyrin domain of GLP-1. cdc10/SWI6/ankyrin motifs have been shown to mediate specific protein-protein interactions in other polypeptides. We propose that the glp-1(ts) mutations disrupt contact between GLP-1 and an as yet unidentified target protein(s) and that the dominant suppressor mutations restore appropriate protein-protein interactions.

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7

Alleva, D. G., C. J. Burger, and K. D. Elgert. "Tumor-induced regulation of suppressor macrophage nitric oxide and TNF-alpha production. Role of tumor-derived IL-10, TGF-beta, and prostaglandin E2." Journal of Immunology 153, no. 4 (August 15, 1994): 1674–86. http://dx.doi.org/10.4049/jimmunol.153.4.1674.

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Abstract In vitro-activated macrophages (Mphi) co-express cytotoxicity for tumor cells and suppression of lymphocyte proliferation. These Mphi functions increase during tumor growth and are mediated by soluble molecules. Because Mphi-derived nitric oxide (NO) and TNF-alpha mediate both cytotoxicity and suppression, we determined whether fibrosarcoma (Meth-KDE) growth increased Mphi-mediated suppression of T cell proliferation by increasing Mphi NO and TNF-alpha production. Tumor-bearing host peritoneal Mphi produced more NO and TNF-alpha than normal host Mphi when activated with IFN-gamma or LPS, respectively. This tumor-induced increase in Mphi NO and TNF-alpha production mediated suppression of alloantigen-driven T cell proliferation, because treatment with either NG-monomethyl-L-arginine or anti-TNF-alpha Ab blocked tumor-bearing host Mphi-mediated suppression. TNF-alpha did not directly suppress T cells, but it induced Mphi NO production that down-regulated proliferation. When non-tumor-infiltrating peritoneal Mphi were cultured with Meth-KDE cell supernatants, Mphi production of NO and TNF-alpha was strongly down-regulated. The tumor-derived molecules responsible for this inhibition were IL-10, TGF-beta 1, and prostaglandin E2. The experimental evidence leading to this conclusion included: 1) The Meth-KDE cells produced significant levels of these cytokines. 2) Recombinant forms of these cytokines suppressed NO and TNF-alpha production. 3) Ab-mediated absorption of these cytokines from tumor cell supernatants restored NO and TNF-alpha production. 4) Anti-IL-10 and anti-TGF-beta 1 Ab addition to IFN-gamma-stimulated Mphi restored NO production. Culture supernatants of two human carcinoma cell lines and another murine fibrosarcoma suppressed Mphi NO and TNF-alpha production, which was partly mediated by TGF-beta 1 and prostaglandin E2. Collectively, these results suggest that tumor growth promotes distal Mphi suppressor activity by increasing Mphi production of cytotoxic molecules and concomitantly down-regulating the local production of these antitumor molecules.

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8

Welshons, W. J., and H. J. Welshons. "ENHANCEMENT AND SUPPRESSION OF A EUCHROMATIC POSITION EFFECT AT NOTCH IN DROSOPHILA." Genetics 113, no. 2 (June 1, 1986): 337–54. http://dx.doi.org/10.1093/genetics/113.2.337.

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ABSTRACT The recessive visible rough-eye mutant facet-strawberry, faswb, is caused by the deletion of 0.8 kb of base sequences from the 5' end of the Notch locus. Visible deficiencies adjacent to faswb suppress this mutant effect of the Notch locus, and in the same region (between salivary bands 3C1 and 3C7), we have demonstrated the presence of at least one partial suppressor and one enhancer of the faswb position effect at Notch.—The enhancer seems to be a small inversion approximately equal to the salivary-band doublet 3C2, 3, and the partial suppressor lies between the inversion in 3C2, 3 and the small deletion in faswb immediately distal to 3C7. Neither the enhancer, e(faswb), nor the partial suppressor, su(faswb), can be detected except when linked in cis to faswb. The e(faswb) and the su(faswb), in unison, act antagonistically on the faswb position effect.—The faswb mutant is interpreted to be a nonvariegating position effect at the Notch locus resulting from a novel euchromatic—euchromatic association of base sequences caused by the small deletion.

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9

Quaresma, Luisa, Antonio CALDEIRA Fradique, Fernanda Cabrita, Alexandra Pupo, Guedes DA Silva, Gualdino Silva, Jorge Esteves, et al. "The prognostic value of P53 in the nodal metastization of gastric cancer." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e14673-e14673. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e14673.

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e14673 Background: Lymph node Metastases play a major role as an independent prognostic factor in gastric cancer. Presence of distal lymph node metastases assumes a pejorative prognostic significance, and represents a problem in terms of therapeutic approach. For this reason it’s of major interest to find predictive markers of distal lymph node chain involvement. The P53 tumor suppressor gene, a product of the TP53 gene works normally as a brake on DNA replication, as suppressor of angiogenesis and triggering of apoptosis. The gene most frequently mutated in gastric cancer is the TP53, that is responsible for the production of P53 mutant protein, which forms inactive complex with the native protein, and manifest by the overexpression of p53 in immunocytochemistry. The overexpression of P53 gene has been considered a bad prognostic factor associated mainly with lymph node metastases. Methods: This study seeks to determine the relation between the expression of P53 and the presence of distal lymph node metastases as an indicator for an extended lymphadenectomy. A total of 50 patients undergoing surgery with D2 lymphadenectomy for gastric carcinoma with curative intent were enrolled in this work. Therefore it was evaluated in 1,786 lymph nodes the correlation between the P53 expression with tumor location, size, histological type, depth , number of nodes involved, number of distal lymph node metastases and the TNM stage. Results: In all parameters, mutant P53 protein related with indicators of poor prognosis. In particular has demonstrated a statistical significant correlation (p=0.019) with the presence of distal lymph node metastases. The main objective of this study which was finding a prognostic predictor of distal nodal metastases has been reached. Conclusions: Mutant P53 protein is a good prognostic indicator, for the presence of distal lymph node involvement in gastric carcinoma.

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10

Nahar, Rahul, Parham Ramezani-Rad, Sinisa Dovat, Maike Buchner, Thomas G. Graeber, and Markus Muschen. "Mechanisms of Ikaros-Mediated Tumor Suppression." Blood 118, no. 21 (November 18, 2011): 408. http://dx.doi.org/10.1182/blood.v118.21.408.408.

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Abstract Abstract 408 Background: The Ikaros (IKZF1) tumor suppressor is deleted in >80% of the cases of Ph+ ALL. While Ikaros cooperates with pre-B cell receptor signaling to induce cell cycle exit in Ph+ ALL (Trageser et al., J Exp Med, 2009), the mechanism of Ikaros-mediated tumor suppression is poorly understood. Here we report on a series of genetic experiments that show that Ikaros (i) interferes with key survival pathways downstream of the BCR-ABL1 kinase, (ii) inhibits leukemia cell proliferation through interaction with the pre-B cell receptor signaling pathway and (iii) activates the tumor suppressors p53, p21 and p27. Results: To elucidate the mechanism of Ikaros-dependent tumor suppression in BCR-ABL1-driven B cell lineage leukemia, we studied regulation of critical phosphorylation events downstream of the BCR-ABL1 kinase as a central mediators of survival and proliferation. Reconstitution of Ikaros expression in BCR-ABL1-transformed pre-B ALL cells resulted in rapid and global dephosphorylation comparable to the effect of Imatinib. A detailed analysis showed that Ikaros-induced dephosphorylation events affect activation of Stat5 (Y694), AKT (S473), ERK1/2 (T202 and Y204) and SRC (Y416). Interestingly, both Imatinib-treatment and reconstitution of pre-B cell receptor signaling using retroviral vectors for expression of the m heavy chain or the BLNK adapter molecule have the same effects as reconstitution of Ikaros. In fact, a comprehensive gene expression analysis demonstrated that Ikaros reconstitution resulted in similar gene expression changes as reconstitution of pre-B cell receptor signaling (m heavy chain or BLNK), reconstitution of PAX5, Cre-mediated deletion of Stat5 or Myc, or treatment with Imatinib. The signature of common gene expression changes shared between reconstitution of Ikaros, Pax5, m heavy chain, BLNK and inducible deletion of Stat5 or Myc and Imatinib-treatment involves known tumor suppressors including SPIB, BTG1, and BTG2. These findings suggest that reconstitution of tumor suppressive transcription factor (Ikaros, Pax5) converges with pre-B cell receptor-mediated tumor suppression. To better understand how pre-B cell receptor signaling and Ikaros intersect, we combined reconstitution of Ikaros with genetic deletion of either the (more proximal) SYK kinase or the (more distal) BLNK adapter molecule. While inducible Cre-mediated deletion of Syk had no effect on Ikaros-mediated tumor suppression, deletion of the BLNK adapter compromised the ability of Ikaros to function as tumor suppressor. These findings were confirmed in an in vivo transplantation experiment. While mice transplanted with Ikaros+ BLNK+ leukemia cells survived indefinitely, mice transplanted with Ikaros- BLNK+, Ikaros+ BLNK- or Ikaros- BLNK- leukemia cells died after 24 to 31 days post transplantation. While these findings provide genetic evidence for collaboration between the Ikaros and pre-B cell receptor tumor suppressor pathways, Ikaros and pre-B cell receptor signaling differ with respect to activation of classical tumor suppressor pathways. While reconstitution of pre-B cell receptor signaling failed to activate Arf, p53 or p27, protein levels of all these molecules were strongly upregulated by Ikaros. In agreement with these findings, reconstitution of pre-B cell receptor signaling had the same tumor suppressive effect in wildtype leukemia cells as in Arf−/−, p53−/− as well as p27−/− leukemia cells. Conversely, deletion of Arf and p53 significantly diminished the ability of Ikaros to function as tumor suppressor. Conclusion: Ikaros deletion represents a near-obligatory lesion in the pathogenesis of Ph+ ALL. Here we provide genetic evidence for three novel pathways of Ikaros-mediated tumor suppression. Like PAX5, Ikaros reconstitution results in multiple dephosphorylation events (Stat5, AKT, ERK1/2 and SRC are affected). In collaboration with the pre-B cell receptor and its downstream adapter molecule BLNK, Ikaros suppressed MYC and inhibits cell cycle progression. Induction of the Arf/p53 pathway represents a distinct function of Ikaros, which is not shared with the pre-B cell receptor signaling pathway. Disclosures: No relevant conflicts of interest to declare.

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11

Wemmer, T., and C. Klämbt. "A genetic analysis of the Drosophila closely linked interacting genes bulge, argos and soba." Genetics 140, no. 2 (June 1, 1995): 629–41. http://dx.doi.org/10.1093/genetics/140.2.629.

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Abstract The Drosophila gene argos encodes a diffusible protein that acts as a negative regulator of cell fate decisions. To define interacting gene products, we performed a genetic analysis of argos, which suggests the presence of several partially redundant gene functions in its immediate vicinity at the chromosomal position 73A. Dose titration experiments have identified two of these loci. One of them corresponds to the gene bulge. Loss of function bulge alleles suppress the rough eye phenotype associated with overexpression of argos; conversely, amorphic argos mutations suppress the eye phenotype seen in flies bearing a single dominant bulge allele. Recombination mapping localized bulge 0.15 cM distal to argos. A second gene, suppressor of bulge and argos (soba), corresponds to the recently described lethal complementation group 73Aj. soba alleles suppress the eye phenotypes seen in flies expressing either the dominant bulge allele or the hs-argos construct. soba resides 120 kb proximal to argos. In addition, we have identified one allele of a new gene, clown, which like soba suppresses the eye phenotypes associated with hs-argos and bulgeDominant. clown maps on chromosome 3 at the cytological position 68CD.

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12

Imanishi, Ayaka, Yuma Aoki, Masaki Kakehi, Shunsuke Mori, Tomomi Takano, Yukihiko Kubota, Hon-Song Kim, Yukimasa Shibata, and Kiyoji Nishiwaki. "Genetic interactions among ADAMTS metalloproteases and basement membrane molecules in cell migration in Caenorhabditis elegans." PLOS ONE 15, no. 12 (December 2, 2020): e0240571. http://dx.doi.org/10.1371/journal.pone.0240571.

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During development of the Caenorhabditis elegans gonad, the gonadal leader cells, called distal tip cells (DTCs), migrate in a U-shaped pattern to form the U-shaped gonad arms. The ADAMTS (a disintegrin and metalloprotease with thrombospondin motifs) family metalloproteases MIG-17 and GON-1 are required for correct DTC migration. Mutations in mig-17 result in misshapen gonads due to the misdirected DTC migration, and mutations in gon-1 result in shortened and swollen gonads due to the premature termination of DTC migration. Although the phenotypes shown by mig-17 and gon-1 mutants are very different from one another, mutations that result in amino acid substitutions in the same basement membrane protein genes, emb-9/collagen IV a1, let-2/collagen IV a2 and fbl-1/fibulin-1, were identified as genetic suppressors of mig-17 and gon-1 mutants. To understand the roles shared by these two proteases, we examined the effects of the mig-17 suppressors on gon-1 and the effects of the gon-1 suppressors and enhancers on mig-17 gonadal defects. Some of the emb-9, let-2 and fbl-1 mutations suppressed both mig-17 and gon-1, whereas others acted only on mig-17 or gon-1. These results suggest that mig-17 and gon-1 have their specific functions as well as functions commonly shared between them for gonad formation. The levels of collagen IV accumulation in the DTC basement membrane were significantly higher in the gon-1 mutants as compared with wild type and were reduced to the wild-type levels when combined with suppressor mutations, but not with enhancer mutations, suggesting that the ability to reduce collagen IV levels is important for gon-1 suppression.

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13

Chung, Leland W. K. "Commentary on Tumor Suppressor Gene, Distal to BRCA-1, in Prostate Cancer." Journal of Urology 155, no. 2 (February 1996): 430–31. http://dx.doi.org/10.1016/s0022-5347(01)66410-3.

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14

Williams, Briana J., Emma Jones, Xiao Lin Zhu, Michael R. Steele, Robert A. Stephenson, L. Ralph Rohr, and Arthur R. Brothman. "Evidence for a Tumor Suppressor Gene Distal to BRCA1 in Prostate Cancer." Journal of Urology 155, no. 2 (February 1996): 720–25. http://dx.doi.org/10.1016/s0022-5347(01)66509-1.

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15

Zhou, Yunli, Xun Zhang, and Anne Klibanski. "MEG3 noncoding RNA: a tumor suppressor." Journal of Molecular Endocrinology 48, no. 3 (March 2, 2012): R45—R53. http://dx.doi.org/10.1530/jme-12-0008.

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Maternally expressed gene 3 (MEG3) is an imprinted gene belonging to the imprinted DLK1–MEG3 locus located at chromosome 14q32.3 in humans. Its mouse ortholog, Meg3, also known as gene trap locus 2 (Gtl2), is located at distal chromosome 12. The MEG3 gene encodes a long noncoding RNA (lncRNA) and is expressed in many normal tissues. MEG3 gene expression is lost in an expanding list of primary human tumors and tumor cell lines. Multiple mechanisms contribute to the loss of MEG3 expression in tumors, including gene deletion, promoter hypermethylation, and hypermethylation of the intergenic differentially methylated region. Re-expression of MEG3 inhibits tumor cell proliferation in culture and colony formation in soft agar. This growth inhibition is partly the result of apoptosis induced by MEG3. MEG3 induces accumulation of p53 (TP53) protein, stimulates transcription from a p53-dependent promoter, and selectively regulates p53 target gene expression. Maternal deletion of the Meg3 gene in mice results in skeletal muscle defects and perinatal death. Inactivation of Meg3 leads to a significant increase in expression of angiogenesis-promoting genes and microvessel formation in the brain. These lines of evidence strongly suggest that MEG3 functions as a novel lncRNA tumor suppressor.

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16

Brunk, B. P., E. C. Martin, and P. N. Adler. "Molecular genetics of the Posterior sex combs/Suppressor 2 of zeste region of Drosophila: aberrant expression of the Suppressor 2 of zeste gene results in abnormal bristle development." Genetics 128, no. 1 (May 1, 1991): 119–32. http://dx.doi.org/10.1093/genetics/128.1.119.

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Abstract We report the molecular characterization of the Posterior sex combs-Suppressor 2 of zeste region of Drosophila melanogaster. The distal breakpoint of the Aristapedioid inversion divides the region into two parts. We have molecularly mapped the lesions associated with several loss of function mutations in the Polycomb group gene Posterior sex combs (Psc) proximal to this breakpoint. In addition, we have found that lesions associated with several loss of function mutations in the Suppressor 2 of zeste [Su(z)2] gene lie distal to this breakpoint. Since the breakpoint does not cause a loss of function in either gene, no essential sequences are shared by these two neighboring genes. There are three dominant gain of function mutations in the region that result in abnormal bristle development. We find that all three juxtapose foreign DNA sequences upstream of the Su(z)2 gene, and that at least two of these mutations (Arp1 and vgD) behave genetically as gain of function mutations in Su(z)2. Northern and in situ hybridization analyses show that the mutations result in increased accumulation of the Su(z)2 mRNA, which we argue is responsible for the bristle loss phenotype.

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17

Martinsson, T., R. M. Sjöberg, K. Hallstensson, M. Nordling, F. Hedborg, and P. Kogner. "Delimitation of a critical tumour suppressor region at distal 1p in neuroblastoma tumours." European Journal of Cancer 33, no. 12 (October 1997): 1997–2001. http://dx.doi.org/10.1016/s0959-8049(97)00278-5.

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18

Försti, Asta, Qianren Jin, Lena Sundqvist, Magnus Söderberg, and Kari Hemminki. "Use of Monozygotic Twins in Search for Breast Cancer Susceptibility Loci." Twin Research 4, no. 4 (August 1, 2001): 251–59. http://dx.doi.org/10.1375/twin.4.4.251.

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AbstractWe have used Swedish monozygotic twins concordant for breast cancer to study genetic changes associated with the development of breast cancer. Because loss of heterozygosity (LOH) at a specific genomic region may reflect the presence of a tumour suppressor gene, loss of the same allele in both of the twins concordant for breast cancer may pinpoint a tumour suppressor gene that confers a strong predisposition to breast cancer. DNA samples extracted from the matched tumour and normal tissues of nine twin pairs were analysed for allelic imbalance using a set of microsatellite markers on chromosomes 1, 13, 16 and 17, containing loci with known tumour suppressor genes. The two main regions, where more twin pairs than expected had lost the same allele, were located at 16qtel, including markers D16S393, D16S305 and D16S413, and at 17p13, distal to the p53 locus. Our results show that the monozygotic twin model can be used to suggest candidate regions of potential tumour suppressor genes, even with a limited number of twin pairs.

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19

Ozturk, Sait, Panagiotis Papageorgis, Chen Khuan Wong, Arthur W. Lambert, Hamid M. Abdolmaleky, Arunthathi Thiagalingam, Herbert T. Cohen, and Sam Thiagalingam. "SDPR functions as a metastasis suppressor in breast cancer by promoting apoptosis." Proceedings of the National Academy of Sciences 113, no. 3 (January 6, 2016): 638–43. http://dx.doi.org/10.1073/pnas.1514663113.

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Metastatic dissemination of breast cancer cells represents a significant clinical obstacle to curative therapy. The loss of function of metastasis suppressor genes is a major rate-limiting step in breast cancer progression that prevents the formation of new colonies at distal sites. However, the discovery of new metastasis suppressor genes in breast cancer using genomic efforts has been slow, potentially due to their primary regulation by epigenetic mechanisms. Here, we report the use of model cell lines with the same genetic lineage for the identification of a novel metastasis suppressor gene, serum deprivation response (SDPR), localized to 2q32-33, a region reported to be associated with significant loss of heterozygosity in breast cancer. In silico metaanalysis of publicly available gene expression datasets suggests that the loss of expression of SDPR correlates with significantly reduced distant-metastasis–free and relapse-free survival of breast cancer patients who underwent therapy. Furthermore, we found that stable SDPR overexpression in highly metastatic breast cancer model cell lines inhibited prosurvival pathways, shifted the balance of Bcl-2 family proteins in favor of apoptosis, and decreased migration and intravasation/extravasation potential, with a corresponding drastic suppression of metastatic nodule formation in the lungs of NOD/SCID mice. Moreover, SDPR expression is silenced by promoter DNA methylation, and as such it exemplifies epigenetic regulation of metastatic breast cancer progression. These observations highlight SDPR as a potential prognostic biomarker and a target for future therapeutic applications.

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Voelker, R. A., S. M. Huang, G. B. Wisely, J. F. Sterling, S. P. Bainbridge, and K. Hiraizumi. "Molecular and genetic organization of the suppressor of sable and minute (1) 1B region in Drosophila melanogaster." Genetics 122, no. 3 (July 1, 1989): 625–42. http://dx.doi.org/10.1093/genetics/122.3.625.

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Abstract Recessive mutations at the suppressor of sable [su(s)] locus in Drosophila melanogaster result in suppression of second site mutations caused by insertions of the mobile element 412. In order to determine whether su(s) mutations might have other phenotypes, a saturation mapping of the su(s) region was carried out. The screen yielded 76 mutations that comprise ten genetic complementation groups ordered distal to proximal as follows: l(1)1Bh, l(1)1Bi, M(1)1B, su(s), l(1)1Bk, l(1)1Ca, mul, tw, l(1)lDa and brc. Twenty-three of the mutations are su(s) alleles, and all are suppressors of the 412-insertion-caused v1 allele. Although the screen could have detected su(s) mutations causing sex-specific dominant lethality or sterility as well as all types of recessive lethality or sterility, the only other phenotype observed was male sterility that is enhanced by cold temperature. This type of sterility is exhibited only by alleles induced by base-substitution-causing mutagens. Genetic functions of the poly(A+) messages transcribed from the su(s) microregion were identified by the reintroduction of cloned sequences into embryos by P element transformation. su(s) function has been attributed to a 5-kb message. The segment of DNA encoding only this 5-kb message rescues both the suppression and cold-sensitive male sterility phenotypes of su(s). Minute (1) 1B has been provisionally identified as encoding a 3.5-kb message; lethal (1)1Bi encodes a 1-kb message; and lethal (1)1Bk encodes a 4-kb message. The possible functions of su(s) and M(1)1B are discussed.

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21

Crossman, M. W., S. M. Hauft, and J. I. Gordon. "The mouse ileal lipid-binding protein gene: a model for studying axial patterning during gut morphogenesis." Journal of Cell Biology 126, no. 6 (September 15, 1994): 1547–64. http://dx.doi.org/10.1083/jcb.126.6.1547.

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Normal, chimeric-transgenic, and transgenic mice have been used to study the axial patterns of ileal lipid-binding protein gene (Ilbp) expression during and after completion of gut morphogenesis. Ilbp is initially activated in enterocytes in bidirectional wave that expands proximally in the ileum and distally to the colon during late gestation and the first postnatal week. This activation occurs at the same time that a wave of cytodifferentiation of the gut endoderm is completing its unidirectional journey from duodenum to colon. The subsequent contraction of Ilbp's expression domain, followed by its reexpansion from the distal to proximal ileum, coincides with a critical period in gut morphogenesis (postnatal days 7-28) when its proliferative units (crypts) form, establish their final stem cell hierarchy, and then multiply through fission. The wave of reactivation is characterized by changing patterns of Ilbp expression: (a) at the proximal most boundary of the wave, villi contain a mixed population of scattered ileal lipid-binding protein (ILBP)-positive and ILBP-negative enterocytes derived from the same monoclonal crypt; (b) somewhat more distally, villi contain vertical coherent stripes of wholly ILBP-positive enterocytes derived from monoclonal crypts and adjacent, wholly ILBP-negative stripes of enterocytes emanating from other monoclonal crypts; and (c) more distally, all the enterocytes on a villus support Ilbp expression. Functional mapping studies of Ilbp's promoter in transgenic mice indicate that nucleotides -145 to +48 contain cis-acting elements sufficient to produce an appropriately directed distal-to-proximal wave of Ilbp activation in the ileum, to maintain an appropriate axial distribution of monophenotypic wholly reporter-positive villi in the distal portion of the ileum, as well as striped and speckled villi in the proximal portion of its expression domain, and to correctly support reporter production in villus-associated ileal enterocytes. Nucleotides -417 to -146 of Ilbp contain a "temporal" suppressor that delays initial ileal activation of the gene until the second postnatal week. Nucleotides -913 to -418 contain a temporal suppressor that further delays initial activation of the gene until the third to fourth postnatal week, a spatial suppressor that prohibits gene expression in the proximal quarter of the ileum and in the proximal colon, and a cell lineage suppressor that prohibits expression in goblet cells during the first two postnatal weeks.

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22

Guan, Xin-Yuan, Jonathan S. T. Sham, Lai-Shan Tai, Yan Fang, Hong Li, and Qiwan Liang. "Evidence for another tumor suppressor gene at 17p13.3 distal to TP53 in hepatocellular carcinoma." Cancer Genetics and Cytogenetics 140, no. 1 (January 2003): 45–48. http://dx.doi.org/10.1016/s0165-4608(02)00654-4.

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23

Hassan, Karl A., Talal Souhani, Ronald A. Skurray, and Melissa H. Brown. "Analysis of Tryptophan Residues in the Staphylococcal Multidrug Transporter QacA Reveals Long-Distance Functional Associations of Residues on Opposite Sides of the Membrane." Journal of Bacteriology 190, no. 7 (January 25, 2008): 2441–49. http://dx.doi.org/10.1128/jb.01864-07.

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ABSTRACT Tryptophan residues can possess a multitude of functions within a multidrug transport protein, e.g., mediating interactions with substrates or distal parts of the protein, or fulfilling a structural requirement, such as guiding the depth of membrane insertion. In this study, the nine tryptophan residues of the staphylococcal QacA multidrug efflux protein were individually mutated to alanine and phenylalanine, and the functional consequences of these changes were determined. Phenylalanine substitutions for each tryptophan residue were functionally tolerated. However, alanine modifications revealed an important functional role for three tryptophan residues, W58, W149, and W173, each of which is well conserved among QacA-related transport proteins in the major facilitator superfamily. The most functionally compromising mutation, an alanine substitution for W58, likely to be located at the extracellular interface of transmembrane segment 2, abolished all detectable QacA-mediated resistance and transport function. Second-site suppressor analyses identified several mutations that rescued the function of the W58A QacA mutant. Remarkably, all of these suppressor mutations were shown to be located in cytoplasmic loops between transmembrane helices 2 and 3 or 12 and 13, demonstrating novel functional associations between amino acid positions on opposite sides of the membrane and in distal N- and C-terminal regions of the QacA protein.

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24

Kim, Nacksung, Jaeseob Kim, Dongkook Park, Christina Rosen, Dale Dorsett, and John Yim. "Structure and Expression of Wild-Type and Suppressible Alleles of the Drosophila purple Gene." Genetics 142, no. 4 (April 1, 1996): 1157–68. http://dx.doi.org/10.1093/genetics/142.4.1157.

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Abstract Viable mutant alleles of purple (pr), such as prbw, exhibit mutant eye colors. This reflects low 6-pyruvoyl tetrahydropterin (PTP) synthase activity required for pigment synthesis. PTP synthase is also required for synthesis of the enzyme cofactor biopterin; presumably this is why some pr alleles are lethal. The prbw eye color phenotype is suppressed by suppressor of sable [su(s)] mutations. The pr gene was cloned to explore the mechanism of this suppression. pr produces two PTP synthase mRNAs: one constitutively from a distal promoter and one in late pupae and young adult heads from a proximal promoter. The latter presumably supports eye pigment synthesis. The prbw allele has a 412 retrotransposon in an intron spliced from both mRNAs. However, the head-specific mRNA is reduced >10-fold in prbw and is restored by a su(s) mutation, while the constitutive transcript is barely affected. The Su(s) protein probably alters processing of RNA containing 412. Because the intron containing 412 is the first in the head-specific mRNA and the second in the constitutive mRNA, binding of splicing machinery to nascent transcripts before the 412 insertion is transcribed may preclude the effects of Su(s) protein.

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25

Chivukula, Mamatha, Leo A. Niemeier, Robert Edwards, Marina Nikiforova, Geetha Mantha, Kim McManus, and Gloria Carter. "Carcinomas of Distal Fallopian Tube and Their Association with Tubal Intraepithelial Carcinoma: Do They Share a Common “Precursor” Lesion? Loss of Heterozygosity and Immunohistochemical Analysis Using PAX 2, WT-1, and P53 Markers." ISRN Obstetrics and Gynecology 2011 (December 15, 2011): 1–8. http://dx.doi.org/10.5402/2011/858647.

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As the role of distal fallopian tube as organ of serous carcinogenesis is emerging, additional literature on the role of tubal intraepithelial carcinoma (TIC) as a precursor lesion in a subset of primary peritoneal serous carcinomas (PPSC is emerging as well. TIC although fallopian tube in origin can be genetically related to ovarian/peritoneal carcinomas. The role of PAX2 in primary fallopian tube carcinomas (PFTC)/PPSC is yet to be defined. The aim of our study was to understand if the biologic properties of tumors arising in the distal fallopian tube that remain as PFTC are different when they seed on to the peritoneal surface (PPSC). A panel of 6 polymorphic microsatellite markers corresponding to p53, PAX2, and WT1 tumor suppressor genes were studied. Invasive carcinomas as well as TIC arising in the distal fallopian tube when remain as PFTC appears to exhibit different LOH patterns in comparison to PPSC. PAX 2 LOH patterns might represent a “hidden PAX 2 signature” analogous to p53 signatures. PAX 2 might be an emerging marker for detection of early serous carcinomas particularly in BRCA + women.

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26

Soparkar, Ketaki, Alfred D. Kinana, Jon W. Weeks, Keith D. Morrison, Hiroshi Nikaido, and Rajeev Misra. "Reversal of the Drug Binding Pocket Defects of the AcrB Multidrug Efflux Pump Protein of Escherichia coli." Journal of Bacteriology 197, no. 20 (August 3, 2015): 3255–64. http://dx.doi.org/10.1128/jb.00547-15.

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ABSTRACTThe AcrB protein ofEscherichia coli, together with TolC and AcrA, forms a contiguous envelope conduit for the capture and extrusion of diverse antibiotics and cellular metabolites. In this study, we sought to expand our knowledge of AcrB by conducting genetic and functional analyses. We began with an AcrB mutant bearing an F610A substitution in the drug binding pocket and obtained second-site substitutions that overcame the antibiotic hypersusceptibility phenotype conferred by the F610A mutation. Five of the seven unique single amino acid substitutions—Y49S, V127A, V127G, D153E, and G288C—mapped in the periplasmic porter domain of AcrB, with the D153E and G288C mutations mapping near and at the distal drug binding pocket, respectively. The other two substitutions—F453C and L486W—were mapped to transmembrane (TM) helices 5 and 6, respectively. The nitrocefin efflux kinetics data suggested that all periplasmic suppressors significantly restored nitrocefin binding affinity impaired by the F610A mutation. Surprisingly, despite increasing MICs of tested antibiotics and the efflux ofN-phenyl-1-naphthylamine, the TM suppressors did not improve the nitrocefin efflux kinetics. These data suggest that the periplasmic substitutions act by influencing drug binding affinities for the distal binding pocket, whereas the TM substitutions may indirectly affect the conformational dynamics of the drug binding domain.IMPORTANCEThe AcrB protein and its homologues confer multidrug resistance in many important human bacterial pathogens. A greater understanding of how these efflux pump proteins function will lead to the development of effective inhibitors against them. The research presented in this paper investigates drug binding pocket mutants of AcrB through the isolation and characterization of intragenic suppressor mutations that overcome the drug susceptibility phenotype of mutations affecting the drug binding pocket. The data reveal a remarkable structure-function plasticity of the AcrB protein pertaining to its drug efflux activity.

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27

Thomas, Marc A., Darren M. Preece, and Jacqueline M. Bentel. "Androgen regulation of the prostatic tumour suppressor NKX3.1 is mediated by its 3′ untranslated region." Biochemical Journal 425, no. 3 (January 15, 2010): 575–83. http://dx.doi.org/10.1042/bj20091109.

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The homeodomain transcription factor NKX3.1 is a prostate-specific tumour suppressor, expression of which is reduced or undetectable in the majority of metastatic prostate tumours. In the normal prostate and in prostate cancer cells, NKX3.1 expression is under tight androgenic control that we have shown to be mediated by its ~2.5 kb 3′UTR (3′ untranslated region). Reporter deletion analysis of the NKX3.1 3′UTR identified three regions that were transactivated by DHT (5α-dihydrotestosterone) in the AR (androgen receptor)-expressing prostate cancer cell line LNCaP. Reversal of DHT effects by the anti-androgen bicalutamide supported an AR-mediated mechanism, and bioinformatic analysis of the NKX3.1 3′UTR identified canonical AREs (androgen-response elements) in each of the androgen-responsive regions. EMSAs (electrophoretic mobility-shift assays) indicated binding of the AR DNA-binding domain to two of the AREs, a proximal ARE at +2378–2392 from the transcription start site, and a more distal ARE at +3098–3112. ChIP (chromatin immunoprecipitation) analysis provided further evidence of ligand-dependent recruitment of endogenous AR to sequence encompassing each of the two elements, and site-directed mutagenesis and deletion analysis confirmed the contribution of each of the AREs in reporter assays. The present studies have therefore demonstrated that the NKX3.1 3′UTR functions as an androgen-responsive enhancer, with the proximal ARE contributing the majority and the distal ARE providing a smaller, but significant, proportion of the androgen responsiveness of the NKX3.1 3′UTR. Characterization of androgen-responsive regions of the NKX3.1 gene will assist in the identification of transcriptional regulatory mechanisms that lead to the deregulation of NKX3.1 expression in advanced prostate cancers.

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28

Liang, Hua Laura, Enyu Rao, Yuzhu Hou, Jiaai Wang, Xiaona Huang, Xianbin Yu, Liangliang Wang, Chuan He, Everett Vokes, and Ralph Weichselbaum. "Induction of Inflammatory Macrophages in Solid Tumors by All-trans Retinoic Acid Augments Radiation Efficacy." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 118.06. http://dx.doi.org/10.4049/jimmunol.208.supp.118.06.

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Abstract Radiotherapy is an important anticancer treatment modality that activates innate and adaptive immune responses. Local RT induces an influx of myeloid cells (mostly myeloid-derived suppressor cells MDSCs), which suppress T-cell function, in the tumor microenvironment (TME). Alleviating therapy-induced immunosuppression would address a significant barrier to the efficacy of current cancer immunotherapeutic approaches. When all-trans retinoic acid (RA) was administered with radiation, we observed superior antitumor responses compared with ionizing radiation (IR) alone or RA alone. The effects of combination treatment were accompanied by a marked increase of tumor necrosis factor–α– (TNFα) and inducible nitric oxide synthase (iNOS)–producing inflammatory macrophages in local and distal nonirradiated tumors. Inflammatory macrophages (Inf-MAC) are essential for the therapeutic efficacy of combination treatment by inducing effector T cell infiltration and enhancing the effector T cell to regulatory T cell ratio in local and distal tumors. T cells and T cell–derived interferon-γ are crucial for increasing inflammatory macrophage levels in IR- and RA-treated tumors. The synergistic positive feedback loop of inflammatory macrophages and adaptive immunity is required for the antitumor efficacy of IR + RA combination treatment. Our findings provide a translational and relatively nontoxic strategy for enhancing the local and systemic antitumor effects of IR. Single cell RNAseq of immune infiltrates revealed unique transcriptional changes delineating the differentiation of Inf-Mac in the TME which may lead to potential specific therapeutic targets.

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29

Yamamoto, M. T., A. Mitchelson, M. Tudor, K. O'Hare, J. A. Davies, and G. L. Miklos. "Molecular and cytogenetic analysis of the heterochromatin-euchromatin junction region of the Drosophila melanogaster X chromosome using cloned DNA sequences." Genetics 125, no. 4 (August 1, 1990): 821–32. http://dx.doi.org/10.1093/genetics/125.4.821.

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Abstract We have used three cloned DNA sequences consisting of (1) part of the suppressor of forked transcription unit, (2) a cloned 359-bp satellite, and (3), a type I ribosomal insertion, to examine the structure of the base of the X chromosome of Drosophila melanogaster where different chromatin types are found in juxtaposition. A DNA probe from the suppressor of forked locus hybridizes exclusively to the very proximal polytenized part of division 20, which forms part of the beta-heterochromatin of the chromocenter. The cloned 359-bp satellite sequence, which derives from the proximal mitotic heterochromatin between the centromere and the ribosomal genes, hybridizes to the under replicated alpha-heterochromatin of the chromocenter. The type I insertion sequence, which has major locations in the ribosomal genes and in the distal mitotic heterochromatin of the X chromosome, hybridizes as expected to the nucleolus but does not hybridize to the beta-heterochromatic division 20 of the polytene X chromosome. Our molecular data reveal that the suppressor of forked locus, which on cytogenetic grounds is the most proximal ordinary gene on the X chromosome, is very close to the junction of the polytenized and non-polytenized region of the X chromosome. The data have implications for the structure of beta-heterochromatin-alpha-heterochromatin junction zones in both mitotic and polytene chromosomes, and are discussed with reference to models of chromosome structure.

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30

Chen, Bo-Shiun, and Michael Hampsey. "Functional Interaction between TFIIB and the Rpb2 Subunit of RNA Polymerase II: Implications for the Mechanism of Transcription Initiation." Molecular and Cellular Biology 24, no. 9 (May 1, 2004): 3983–91. http://dx.doi.org/10.1128/mcb.24.9.3983-3991.2004.

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ABSTRACT The general transcription factor TFIIB is required for accurate initiation, although the mechanism by which RNA polymerase II (RNAP II) identifies initiation sites is not well understood. Here we describe results from genetic and biochemical analyses of an altered form of yeast TFIIB containing an arginine-78 → cysteine (R78C) replacement in the “B-finger” domain. TFIIB R78C shifts start site selection downstream of normal and confers a cold-sensitive growth defect (Csm−). Suppression of the R78C Csm− phenotype identified a functional interaction between TFIIB and the Rpb2 subunit of RNAP II and defined a novel role for Rpb2 in start site selection. The rpb2 suppressor encodes a glycine-369 → serine (G369S) replacement, located in the “lobe” domain of Rpb2 and near the Rpb9 subunit, which was identified previously as an effector of start site selection. The Rpb2-Rpb9 “lobe-jaw” region of RNAP II is downstream of the catalytic center and distal to the site of RNAP II-TFIIB interaction. A TFIIB R78C mutant extract was defective for promoter-specific run-on transcription but yielded an altered pattern of abortive initiation products, indicating that the R78C defect does not preclude initiation. The sua7-3 rpb2-101 double mutant was sensitive to 6-azauracil in vivo and to nucleoside triphosphate substrate depletion in vitro. In the context of the recent X-ray structure of the yeast RNAP II-TFIIB complex, these results define a functional interaction between the B-finger domain of TFIIB and the distal lobe-jaw region of RNAP II and provide insight into the mechanism of start site selection.

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31

Behboudi, A., C. Nordlander, K. Klinga-Levan, and S. Karlsson. "320 POSTER Evidence for a tumor suppressor locus distal to Tp53 – a study in experimental endometrial adenocarcinoma." European Journal of Cancer Supplements 5, no. 4 (September 2007): 62. http://dx.doi.org/10.1016/s1359-6349(07)70338-5.

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32

Nordlander, Carola, Sandra Karlsson, Åsa Karlsson, Åsa Sjöling, Marta Winnes, Karin Klinga-Levan, and Afrouz Behboudi. "Analysis of chromosome 10 aberrations in rat endometrial cancer-evidence for a tumor suppressor locus distal toTp53." International Journal of Cancer 120, no. 7 (January 23, 2007): 1472–81. http://dx.doi.org/10.1002/ijc.22533.

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33

Guzy, Robert D., Bhumika Sharma, Eric Bell, Navdeep S. Chandel, and Paul T. Schumacker. "Loss of the SdhB, but Not the SdhA, Subunit of Complex II Triggers Reactive Oxygen Species-Dependent Hypoxia-Inducible Factor Activation and Tumorigenesis." Molecular and Cellular Biology 28, no. 2 (October 29, 2007): 718–31. http://dx.doi.org/10.1128/mcb.01338-07.

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ABSTRACT Mitochondrial complex II is a tumor suppressor comprised of four subunits (SdhA, SdhB, SdhC, and SdhD). Mutations in any of these should disrupt complex II enzymatic activity, yet defects in SdhA produce bioenergetic deficiency while defects in SdhB, SdhC, or SdhD induce tumor formation. The mechanisms underlying these differences are not known. We show that the inhibition of distal subunits of complex II, either pharmacologically or via RNA interference of SdhB, increases normoxic reactive oxygen species (ROS) production, increases hypoxia-inducible factor alpha (HIF-α) stabilization in an ROS-dependent manner, and increases growth rates in vitro and in vivo without affecting hypoxia-mediated activation of HIF-α. Proximal pharmacologic inhibition or RNA interference of complex II at SdhA, however, does not increase normoxic ROS production or HIF-α stabilization and results in decreased growth rates in vitro and in vivo. Furthermore, the enhanced growth rates resulting from SdhB suppression are inhibited by the suppression of HIF-1α and/or HIF-2α, indicating that the mechanism of SdhB-induced tumor formation relies upon ROS production and subsequent HIF-α activation. Therefore, differences in ROS production, HIF proliferation, and cell proliferation contribute to the differences in tumor phenotype in cells lacking SdhB as opposed to those lacking SdhA.

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34

Erben, Reinhold G. "Pleiotropic Actions of FGF23." Toxicologic Pathology 45, no. 7 (October 2017): 904–10. http://dx.doi.org/10.1177/0192623317737469.

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Fibroblast growth factor-23 (FGF23) is a bone-derived hormone, mainly produced by osteoblasts and osteocytes in response to increased extracellular phosphate and circulating vitamin D hormone. Endocrine FGF23 signaling requires co-expression of the ubiquitously expressed FGF receptor 1 (FGFR1) and the co-receptor α-Klotho (Klotho). In proximal renal tubules, FGF23 suppresses the membrane expression of the sodium–phosphate cotransporters Npt2a and Npt2c which mediate urinary reabsorption of filtered phosphate. In addition, FGF23 suppresses proximal tubular expression of 1α-hydroxylase, the key enzyme responsible for vitamin D hormone production. In distal renal tubules, FGF23 signaling activates with-no-lysine kinase 4, leading to increased renal tubular reabsorption of calcium and sodium. Therefore, FGF23 is not only a phosphaturic but also a calcium- and sodium-conserving hormone, a finding that may have important implications for the pathophysiology of chronic kidney disease. Besides these endocrine, Klotho-dependent functions of FGF23, FGF23 is also an auto-/paracrine suppressor of tissue-nonspecific alkaline phosphatase transcription via Klotho-independent FGFR3 signaling, leading to local inhibition of mineralization through accumulation of pyrophosphate. In addition, FGF23 may target the heart via an FGFR4-mediated Klotho-independent signaling cascade. Taken together, there is emerging evidence that FGF23 is a pleiotropic hormone, linking bone with several other organ systems.

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35

Murthy, Vanishree, Luciana A. Haddad, Nicole Smith, Denise Pinney, Robert Tyszkowski, Dennis Brown, and Vijaya Ramesh. "Similarities and differences in the subcellular localization of hamartin and tuberin in the kidney." American Journal of Physiology-Renal Physiology 278, no. 5 (May 1, 2000): F737—F746. http://dx.doi.org/10.1152/ajprenal.2000.278.5.f737.

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Tuberous sclerosis complex (TSC) is an autosomal dominant disorder characterized by hamartomas in multiple organs, notably the brain and kidneys. The disease is caused by mutations in TSC1or TSC2 genes, coding hamartin and tuberin, respectively. Immunofluorescence analysis of tuberin and hamartin performed here demonstrates that both proteins are specifically expressed in the distal urinary tubule, comprising the distal tubules, connecting segment, and collecting ducts. Hamartin, distinct from tuberin, is expressed in the thick ascending limbs of Henle and in juxtaglomerular cells, where it colocalizes with renin. In positive epithelial cells, tuberin localizes to the cytoplasm as well as the apical membrane. Hamartin, however, preferentially localizes to the apical membrane. The two proteins colocalize at the apical membrane of type A intercalated cells and connecting tubule cells, whereas in type B intercalated cells they reveal a variable pattern of expression. The cell-specific expression of tuberin and hamartin described here will provide critical insight into the cell types that give rise to kidney lesions, and the tumor suppressor role of these proteins in TSC.

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36

Tsuchiya, Eiju, Akira Tanigami, Yuichi Ishikawa, Kazunori Nishida, Moriaki Hayashi, Yoshio Tokuchi, Takehisa Hashimoto, Sakae Okumura, Shigehiro Tsuchiya, and Ken Nakagawa. "Three New Regions on Chromosome 17p13.3 Distal to p53 with Possible Tumor Suppressor Gene Involvement in Lung Cancer." Japanese Journal of Cancer Research 91, no. 6 (June 2000): 589–96. http://dx.doi.org/10.1111/j.1349-7006.2000.tb00986.x.

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37

Hubbard-Smith, K., P. Patsalis, J. R. Pardinas, K. K. Jha, A. S. Henderson, and H. L. Ozer. "Altered chromosome 6 in immortal human fibroblasts." Molecular and Cellular Biology 12, no. 5 (May 1992): 2273–81. http://dx.doi.org/10.1128/mcb.12.5.2273-2281.1992.

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Human diploid fibroblasts have a limited life span in vitro, and spontaneous immortalization is an extremely rare event. We have used transformation of human diploid fibroblasts by an origin-defective simian virus 40 genome to develop series of genetically matched immortal cell lines to analyze immortalization. Comparison of a preimmortal transformant (SVtsA/HF-A) with its uncloned and cloned immortalized derivatives (AR5 and HAL) has failed to reveal any major alteration involving the simian virus 40 genome. Karyotypic analysis, however, demonstrated that all of the immortal cell lines in this series have alterations of chromosome 6 involving loss of the portion distal to 6q21. The karyotypic analysis was corroborated by DNA analyses. Southern analysis demonstrated that only one copy of three proto-oncogene loci (ros1, c-myb, and mas1) on 6q was retained in immortal cells. Polymerase chain reaction analysis of the microsatellite polymorphism at 6q22 (D6S87) showed loss of heterozygosity. In addition, elevated expression of c-myb (6q22-23) was observed. We hypothesize that the region at and/or distal to 6q21 plays a role in immortalization, consistent with the presence of a growth suppressor gene.

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38

Hubbard-Smith, K., P. Patsalis, J. R. Pardinas, K. K. Jha, A. S. Henderson, and H. L. Ozer. "Altered chromosome 6 in immortal human fibroblasts." Molecular and Cellular Biology 12, no. 5 (May 1992): 2273–81. http://dx.doi.org/10.1128/mcb.12.5.2273.

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Анотація:

Human diploid fibroblasts have a limited life span in vitro, and spontaneous immortalization is an extremely rare event. We have used transformation of human diploid fibroblasts by an origin-defective simian virus 40 genome to develop series of genetically matched immortal cell lines to analyze immortalization. Comparison of a preimmortal transformant (SVtsA/HF-A) with its uncloned and cloned immortalized derivatives (AR5 and HAL) has failed to reveal any major alteration involving the simian virus 40 genome. Karyotypic analysis, however, demonstrated that all of the immortal cell lines in this series have alterations of chromosome 6 involving loss of the portion distal to 6q21. The karyotypic analysis was corroborated by DNA analyses. Southern analysis demonstrated that only one copy of three proto-oncogene loci (ros1, c-myb, and mas1) on 6q was retained in immortal cells. Polymerase chain reaction analysis of the microsatellite polymorphism at 6q22 (D6S87) showed loss of heterozygosity. In addition, elevated expression of c-myb (6q22-23) was observed. We hypothesize that the region at and/or distal to 6q21 plays a role in immortalization, consistent with the presence of a growth suppressor gene.

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39

Wei, Lingmin, Shaoying Wen, Zhonghua Tu, Yanqing Zhao, and Huogen Li. "Overexpression of Liriodendron tulipifera JAG Gene (LtuJAG) Changes Leaf Shapes in Transgenic Arabidopsis thaliana." International Journal of Molecular Sciences 23, no. 3 (January 25, 2022): 1322. http://dx.doi.org/10.3390/ijms23031322.

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In Arabidopsis thaliana, JAGGED (JAG) is a transcription inhibitor that controls the development of leaf polarity and regulates the expression of genes controlling lateral organ formation. Liriodendron tulipifera is an ornamental tree with extraordinary tulip-shaped flowers and goose web-like leaves, this is one of the suitable plants for morphological development research. To investigate the potential functions of the LtuJAG gene, we isolated the full-length LtuJAG from L. tulipifera, transferred it into A. thaliana via agrobacterium-mediated transformation, and monitored its expression pattern. Subcellular localization showed that LtuJAG was located in the nucleus. RT-qPCR assays indicated that LtuJAG was expressed mainly in leaf buds and flowers, but not in mature leaves and stems. GUS staining results showed that LtuJAG was expressed in the shoot apical meristem (SAM). Overexpressing LtuJAG changed A. thaliana leaf shapes, causing a moderate serration and a slight asymmetric distribution in the medio-lateral and proximal-distal axes. Ectopic expression of LtuJAG induced the expression of lateral organ boundary suppressors JAGGED LATERAL ORGANS (JLO) and ARABIDOPSIS THALIANA HOMEOBOX1 (ATH1). It also repressed the expression of the apical meristem suppressor class-1 KNOX gene (KNOX I) and altered endogenous hormone levels. Our results suggest that LtuJAG plays a role in negatively regulating leaf polarity formation in L. tulipifera.

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40

Wu, C. T., and M. Howe. "A genetic analysis of the Suppressor 2 of zeste complex of Drosophila melanogaster." Genetics 140, no. 1 (May 1, 1995): 139–81. http://dx.doi.org/10.1093/genetics/140.1.139.

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Abstract The zeste1 (z1) mutation of Drosophila melanogaster produces a mutant yellow eye color instead of the wild-type red. Genetic and molecular data suggest that z1 achieves this change by altering expression of the wild-type white gene in a manner that exhibits transvection effects. There exist suppressor and enhancer mutations that modify the z1 eye color, and this paper summarizes our studies of those belonging to the Suppressor 2 of zeste complex [Su(z)2-C]. The Su(z)2-C consists of at least three subregions called Psc (Posterior sex combs), Su(z)2 and Su(z)2D (Distal). The products of these subregions are proposed to act at the level of chromatin. Complementation analyses predict that the products are functionally similar and interacting. The alleles of Psc define two overlapping phenotypic classes, the hopeful and hapless. The distinctions between these two classes and the intragenic complementation seen among some of the Psc alleles are consistent with a multidomain structure for the product of Psc. Psc is a member of the homeotic Polycomb group of genes. A general discussion of the Polycomb and trithorax group of genes, position-effect variegation, transvection, chromosome pairing and chromatin structure is presented.

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41

Ejeskär, K., H. Aburatani, J. Abrahamsson, P. Kogner, and T. Martinsson. "Loss of heterozygosity of 3p markers in neuroblastoma tumours implicate a tumour-suppressor locus distal to the FHIT gene." British Journal of Cancer 77, no. 11 (June 1998): 1787–91. http://dx.doi.org/10.1038/bjc.1998.297.

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42

Kim, J., B. Shen, C. Rosen, and D. Dorsett. "The DNA-binding and enhancer-blocking domains of the Drosophila suppressor of Hairy-wing protein." Molecular and Cellular Biology 16, no. 7 (July 1996): 3381–92. http://dx.doi.org/10.1128/mcb.16.7.3381.

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Mutations in the suppressor of Hairy-wing [su(Hw)] gene of Drosophila melanogaster can cause female sterility and suppress mutations that are insertions of the gypsy retrotransposon. Gypsy binds the protein (SUHW) encoded by su(Hw), and SUHW prevents enhancers promoter-distal to gypsy from activating gene transcription. SUHW contains 12 zinc fingers flanked by acidic N- and C-terminal domains. We examined the roles of each of the 12 zinc fingers in binding gypsy DNA and classified them into four groups: essential (fingers 6 through 10); beneficial but nonessential (fingers 1, 2, 3, and 11); unimportant (fingers 5 and 12); and inhibitory (finger 4). Because finger 10 is not required for female fertility but is essential for binding gypsy, these results imply that the SUHW-binding sites required for oogenesis differ in sequence from the gypsy-binding sites. We also examined the functions of the N- and C-terminal domains of SUHW by determining the ability of various deletion mutants to support female fertility and to alter expression of gypsy insertion alleles of the yellow, cut, forked, and Ultrabithorax genes. No individual segment of the N- and C-terminal domains of SUHW is absolutely required to alter expression of gypsy insertion alleles. However, the most important domain lies between residues 737 and 880 in the C-terminal domain. This region also contains the residues required for female fertility, and the fertility domain may be congruent with the enhancer-blocking domain. These results imply that SUHW blocks different enhancers and supports oogenesis by the same or closely related molecular mechanisms.

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43

Bender, A., and J. R. Pringle. "Use of a screen for synthetic lethal and multicopy suppressee mutants to identify two new genes involved in morphogenesis in Saccharomyces cerevisiae." Molecular and Cellular Biology 11, no. 3 (March 1991): 1295–305. http://dx.doi.org/10.1128/mcb.11.3.1295-1305.1991.

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Genes CDC24 and CDC42 are required for the establishment of cell polarity and for bud formation in Saccharomyces cerevisiae. Temperature-sensitive (Ts-) mutations in either of these genes cause arrest as large, unbudded cells in which the nuclear cycle continues. MSB1 was identified previously as a multicopy suppressor of Ts- cdc24 and cdc42 mutations. We have now sequenced MSB1 and constructed a deletion of this gene. The predicted amino acid sequence does not closely resemble any other in the available data bases, and the deletion does not produce any readily detectable phenotype. However, we have used a colony-sectoring assay to identify additional genes that appear to interact with MSB1 and play a role in bud emergence. Starting with a strain deleted for the chromosomal copy of MSB1 but containing MSB1 on a high-copy-number plasmid, mutants were identified in which MSB1 had become essential for viability. The new mutations defined two genes, BEM1 and BEM2; both the bem1 and bem2 mutations are temperature sensitive and are only partially suppressed by MSB1. In bem1 cells, a single copy of MSB1 is necessary and sufficient for viability at 23 or 30 degrees C, but even multiple copies of MSB1 do not fully suppress the growth defect at 37 degrees C. In bem2 cells, a single copy of MSB1 is necessary and sufficient for viability at 23 degrees C, multiple copies are necessary for viability at 30 degrees C, and even multiple copies of MSB1 do not suppress the growth defect at 37 degrees C. In a wild-type background (i.e., a single chromosomal copy of MSB1), both bem1 and bem2 mutations cause cells to become large and multinucleate even during growth at 23 degrees C, suggesting that these genes are involved in bud emergence. This suggestion is supported for BEM1 by other evidence obtained in a parallel study (J. Chant, K. Corrado, J. Pringle, and I. Herskowitz, submitted for publication). BEM1 maps centromere distal to TYR1 on chromosome II, and BEM2 maps between SPT15 and STP2 on chromosome V.

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44

Bender, A., and J. R. Pringle. "Use of a screen for synthetic lethal and multicopy suppressee mutants to identify two new genes involved in morphogenesis in Saccharomyces cerevisiae." Molecular and Cellular Biology 11, no. 3 (March 1991): 1295–305. http://dx.doi.org/10.1128/mcb.11.3.1295.

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Genes CDC24 and CDC42 are required for the establishment of cell polarity and for bud formation in Saccharomyces cerevisiae. Temperature-sensitive (Ts-) mutations in either of these genes cause arrest as large, unbudded cells in which the nuclear cycle continues. MSB1 was identified previously as a multicopy suppressor of Ts- cdc24 and cdc42 mutations. We have now sequenced MSB1 and constructed a deletion of this gene. The predicted amino acid sequence does not closely resemble any other in the available data bases, and the deletion does not produce any readily detectable phenotype. However, we have used a colony-sectoring assay to identify additional genes that appear to interact with MSB1 and play a role in bud emergence. Starting with a strain deleted for the chromosomal copy of MSB1 but containing MSB1 on a high-copy-number plasmid, mutants were identified in which MSB1 had become essential for viability. The new mutations defined two genes, BEM1 and BEM2; both the bem1 and bem2 mutations are temperature sensitive and are only partially suppressed by MSB1. In bem1 cells, a single copy of MSB1 is necessary and sufficient for viability at 23 or 30 degrees C, but even multiple copies of MSB1 do not fully suppress the growth defect at 37 degrees C. In bem2 cells, a single copy of MSB1 is necessary and sufficient for viability at 23 degrees C, multiple copies are necessary for viability at 30 degrees C, and even multiple copies of MSB1 do not suppress the growth defect at 37 degrees C. In a wild-type background (i.e., a single chromosomal copy of MSB1), both bem1 and bem2 mutations cause cells to become large and multinucleate even during growth at 23 degrees C, suggesting that these genes are involved in bud emergence. This suggestion is supported for BEM1 by other evidence obtained in a parallel study (J. Chant, K. Corrado, J. Pringle, and I. Herskowitz, submitted for publication). BEM1 maps centromere distal to TYR1 on chromosome II, and BEM2 maps between SPT15 and STP2 on chromosome V.

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45

Klein, Karin G., and Noel P. Bouck. "The distal region of the long arm of human chromosome 1 carries tumor suppressor activity for a human fibrosarcoma line." Cancer Genetics and Cytogenetics 73, no. 2 (April 1994): 109–21. http://dx.doi.org/10.1016/0165-4608(94)90194-5.

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46

Jeddi, Farhad, Shahriar Alipour, Nowruz Najafzadeh, Mehdi Dadashpour, Farhad Pouremamali, Mohammad Reza Sadeghi, Nasser Samadi, Narges Soozangar, and Amir Mahdi Khamaneh. "Reduced Levels of miR–28 and miR–200a Act as Predictor Biomarkers of Aggressive Clinicopathological Characteristics in Gastric Cancer Patients." Galen Medical Journal 8 (January 25, 2019): 1329. http://dx.doi.org/10.31661/gmj.v8i0.1329.

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Background: MicroRNAs (miRNAs) play critical roles in different pathological processes including cancer development and progression. To find novel molecular diagnostic and prognostic markers and promising therapeutic tools for gastric cancer (GC), we aimed to investigate the relationship of the expression levels of miR–28–5p or miR–200a–3p with the clinicopathological criteria and to explore their impacts on the progression of human GC. Materials and Methods: Quantitative RT–PCR was performed to analyze miR–28 and miR–200a expression in 60 GC and 60 non–GC tissue samples. Result: Our results revealed that the expressions of miR–200a and miR–28 were significantly downregulated in GC in comparison with non–GC tissues. Tumors with low miR–28 expression had larger tumor size, more advanced histological grade, and a higher incidence of lymph node and distal metastasis than the tumors with high miR–28 expressions. Furthermore, receiver operating characteristic (ROC) analyses demonstrate that the expression of miR–28 is a predictive biomarker allows predicting the histological grade, tumor size, and occurrence of nodal and distal metastases. We also found a significant inverse association between miR–200a expression and the rate of lymph node metastasis (p = 0.010, r = –0.334). Conclusion: Our findings suggest that the miR–28 and miR–200a have tumor–suppressor functions and may be considered as potential biomarkers for gastric cancer diagnosis and prognosis.[GMJ.2018;impress]

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47

Fioretos, Thoas, Bodil Strömbeck, Therese Sandberg, Bertil Johansson, Rolf Billström, Åke Borg, Per-Gunnar Nilsson, et al. "Isochromosome 17q in Blast Crisis of Chronic Myeloid Leukemia and in Other Hematologic Malignancies Is the Result of Clustered Breakpoints in 17p11 and Is Not Associated With Coding TP53 Mutations." Blood 94, no. 1 (July 1, 1999): 225–32. http://dx.doi.org/10.1182/blood.v94.1.225.413k24_225_232.

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An isochromosome of the long arm of chromosome 17, i(17q), is the most frequent genetic abnormality observed during the disease progression of Philadelphia chromosome–positive chronic myeloid leukemia (CML), and has been described as the sole anomaly in various other hematologic malignancies. The i(17q) hence plays a presumably important pathogenetic role both in leukemia development and progression. This notwithstanding, the molecular consequences of this abnormality have not been investigated in detail. We have analyzed 21 hematologic malignancies (8 CML in blast crisis, 8 myelodysplastic syndromes [MDS], 2 acute myeloid leukemias, 2 chronic lymphocytic leukemias, and 1 acute lymphoblastic leukemia) with i(17q) by fluorescence in situ hybridization (FISH). Using a yeast artificial chromosome (YAC) contig, derived from the short arm of chromosome 17, all cases were shown to have a breakpoint in 17p. In 12 cases, the breaks occurred within the Smith-Magenis Syndrome (SMS) common deletion region in 17p11, a gene-rich region which is genetically unstable. In 10 of these 12 cases, we were able to further map the breakpoints to specific markers localized within a single YAC clone. Six other cases showed breakpoints located proximally to the SMS common deletion region, but still within 17p11, and yet another case had a breakpoint distal to this region. Furthermore, using chromosome 17 centromere-specific probes, it could be shown that the majority of the i(17q) chromosomes (11 of 15 investigated cases) were dicentric, ie, they contained two centromeres, strongly suggesting that i(17q) is formed through an intrachromosomal recombination event, and also implicating that the i(17q), in a formal sense, should be designated idic(17)(p11). Because i(17q) formation results in loss of 17p material, potentially uncovering the effect of a tumor suppressor on the remaining 17p, the occurrence of TP53 mutations was studied in 17 cases by sequencing the entire coding region. In 16 cases, noTP53 mutations were found, whereas one MDS displayed a homozygous deletion of TP53. Thus, our data suggest that there is no association between i(17q) and coding TP53 mutations, and that another tumor suppressor gene(s), located in proximity of the SMS common deletion region, or in a more distal location, is of pathogenetic importance in i(17q)-associated leukemia.

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48

Klein, T., and J. A. Campos-Ortega. "klumpfuss, a Drosophila gene encoding a member of the EGR family of transcription factors, is involved in bristle and leg development." Development 124, no. 16 (August 15, 1997): 3123–34. http://dx.doi.org/10.1242/dev.124.16.3123.

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The klumpfuss (klu) transcription unit in Drosophila gives rise to two different transcripts of 4.5 and 4.9 kb, both of which encode a putative transcription factor with four zinc-finger motifs of the C2H2 class. Zinc-finger 2–4 are homologous to those of the proteins of the EGR transcription factor family. As in the case of the most divergent member of the family, the Wilms' tumor suppressor gene (WT-1), klu contains an additional zinc finger, which is only distantly related. Loss of klumpfuss function is semilethal and causes a variety of defects in bristles and legs of adults, as well as in mouth hooks and brains of larvae. Analysis of the mutants indicates that klumpfuss is required for proper specification and differentiation of a variety of cells, including the sensory organ mother cells and those of the distal parts of tarsal segments.

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49

Konishi, Hiroyuki, Miyabi Sugiyama, Kotaro Mizuno, Hiroko Saito, Yasushi Yatabe, Toshitada Takahashi, Hirotaka Osada, and Takashi Takahashi. "Detailed characterization of a homozygously deleted region corresponding to a candidate tumor suppressor locus at distal 17p13.3 in human lung cancer." Oncogene 22, no. 12 (March 2003): 1892–905. http://dx.doi.org/10.1038/sj.onc.1206304.

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50

Lassus, Heini, Reijo Salovaara, Lauri A. Aaltonen, and Ralf Butzow. "Allelic Analysis of Serous Ovarian Carcinoma Reveals Two Putative Tumor Suppressor Loci at 18q22-q23 Distal to SMAD4, SMAD2, and DCC." American Journal of Pathology 159, no. 1 (July 2001): 35–42. http://dx.doi.org/10.1016/s0002-9440(10)61670-7.

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