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Relevant bibliographies by topics / Chromosome 6

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Academic literature on the topic 'Chromosome 6'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 January 2023

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Journal articles on the topic "Chromosome 6"

1

Hausmann, Michael, C. Paul Popescu, Jeannine Boscher, Dominique Kerboœf, Jürgen Dölle, and Christoph Cremer. "Identification and Cytogenetic Analysis of an Abnormal Pig Chromosome for Flow Cytometry and Sorting." Zeitschrift für Naturforschung C 48, no. 7-8 (August 1, 1993): 645–53. http://dx.doi.org/10.1515/znc-1993-7-819.

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Abstract For cytogenetics of pig (Sus scrofa domestica) and the influence of chromosome aberrations on pig production, high interest exists in flow sorted chromosomes for gene mapping, to establish DNA-libraries, or to produce DNA-probes. Flow karyotyping and sorting as well as slit scan flow analysis of metaphase chromosomes of an abnormal cell type carrying a translocation marker chromosome 6/15 are described. Flow sorting of the largest chromosomes of these cells was performed. After sorting the chromosomes still had a well preserved morphology and were identified microscopically by G-banding. The quality of the band pattern of the sorted chromosomes was compatible to that of isolated chromosomes not subjected to flow cytometry. The sorted fraction showed an enrichment of chromosom e 6/15 and chromosome 1 which have quantitatively about the same integrated fluorescence intensity. Slit scan flow analysis was performed to discriminate these two chromosomes. Metacentric and submetacentric chromosom es were analyzed according to their bimodal slit scan profiles. Profiles of the largest chromosomes were distinguished by their different centromeric indices. Two groups were interpreted as the normal chromosome 1 and the translocation chromosom e 6/15.

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Fan, Haitao, Zhe Liu, Peng Zhan, and Guoliang Jia. "Pericentric inversion of chromosome 6 and male fertility problems." Open Medicine 17, no. 1 (January 1, 2022): 191–96. http://dx.doi.org/10.1515/med-2022-0411.

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Abstract As a significant chromosomal structural abnormality, chromosomal inversion is closely related to male infertility. For inversion carriers, the interchromosomal effect explains male infertility, but its specific mechanism remains unclear. Additionally, inversion carriers with different chromosomes have different clinical manifestations. Therefore, genetic counseling is difficult in clinical practice. Herein, four male carriers of pericentric inversion in chromosome 6 have been described. Two patients showed asthenospermia, one showed azoospermia, and the wife of the remaining patient had recurrent miscarriages. Through a literature search, the association between the breakpoint of pericentric inversion in chromosome 6 and male fertility problems are also discussed in this study. Overall, important genes related to asthenospermia in chromosome 6p21 were found, which may be related to the clinical phenotype. These results suggest that physicians should focus on the breakpoints of inversion in genetic counseling.

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Ganguly, Bani Bandana, Vijay Kadam, and Nitin N. Kadam. "Clinical Expression of an Inherited Unbalanced Translocation in Chromosome 6." Case Reports in Genetics 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/396450.

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Unbalanced chromosomal rearrangements are not common; however, they have a significant clinical expression. The parental balanced translocation produces unbalanced chromosome, which is transmitted to next generation through fertilization of gametes carrying the derivative chromosome. The carriers of balanced rearrangements mostly do not have recognizable phenotypic expression. We report a family comprising of healthy and non-consanguineous young parents and their preemie newborn severely affected with congenital anomalies and systemic disorders. Conventional Gbanding analysis of somatic chromosomes identified a balanced translocation, t(6;10)(p23;q24), in mother and an unbalanced rearrangement, der(6)t(6:10)(p23;q24)mat, in the child. The child has inherited a derivative chromosome 6 with partial deletion of 6(p23-pter) and partial trisomy 10(q24-qter), which has resulted in fusion of genes of two different chromosomes. The prominent phenotypic features of del(6p), including high forehead, flat nasal bridge, agenesis of left ear, atrial septal defect (ASD), craniosynostosis, and growth retardation, are overlapping with specific Axenfeld-Reiger-, Larsen-, and Ritscher-Sinzel/3-C syndromes, however, lacking in ocular anomalies, skeletal laxity, or cerebellar malformation. Therefore, this paper rules out the isolated effect of del(6p23) or trisomy 10(q24) on distinct previously reported syndromes and proposes the combined effect of unbalanced chromosomal alteration.

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Mo, Kevin, Teagan Tran, Arjina Boodaghian, John Wear, John Ho, Clark Robin, and Mitchell Goldstein. "An Unbalanced Translocation Involving Partial Duplication of Chromosome 6 and Partial Deletion of Chromosome 10 in a Premature Infant with Tetralogy of Fallot." Neonatology Today 15, no. 9 (September 20, 2020): 20–25. http://dx.doi.org/10.51362/neonatology.today/202091592025.

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Purpose: To report a case of simultaneous chromosome 10 partial deletion and chromosome 6 partial duplication in a preterm infant. Methods: This is a retrospective case report followed with clinical observation, echocardiogram, and genetic testing. Results: A neonate with Tetralogy of Fallot, clubbed feet, low set ears, and webbed neck was found to have chromosomal abnormalities that are consistent with unbalanced translocation between chromosomes 6 and 10, resulting in a partial duplication of chromosome 6 and partial deletion of chromosome 10. Discussion: Chromosome microarray testing in a patient with multiple congenital anomalies can facilitate rapid diagnosis and treatment with the potential to improve the management of complications and subsequent development.

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Ogata, T., D. Ayusawa, M. Namba, E. Takahashi, M. Oshimura, and M. Oishi. "Chromosome 7 suppresses indefinite division of nontumorigenic immortalized human fibroblast cell lines KMST-6 and SUSM-1." Molecular and Cellular Biology 13, no. 10 (October 1993): 6036–43. http://dx.doi.org/10.1128/mcb.13.10.6036-6043.1993.

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Using nontumorigenic immortalized human cell lines KMST-6 (KMST) and SUSM-1 (SUSM), we attempted to identify the chromosome that carries a putative senescence-related gene(s). These cell lines are the only ones that have been established independently from normal human diploid fibroblasts following in vitro mutagenesis. We first examined restriction fragment length polymorphisms on each chromosome of these immortalized cell lines and their parental cell lines and found specific chromosomal alterations common to these cell lines (a loss of heterozygosity in KMST and a deletion in SUSM) on the long arm of chromosome 7. In addition to these, we also found that introduction of chromosome 7 into these cell lines by means of microcell fusion resulted in the cessation of cell division, giving rise to cells resembling cells in senescence. Introduction of other chromosomes, such as chromosomes 1 and 11, on which losses of heterozygosity were also detected in one of the cell lines (KMST), to either KMST or SUSM cells or of chromosome 7 to several tumor-derived cell lines had no effect on their division potential. These results strongly suggest that a gene(s) affecting limited-division potential or senescence of normal human fibroblasts is located on chromosome 7, probably at the long arm of the chromosome, representing the first case in which a specific chromosome reverses the immortal phenotype of otherwise normal human cell lines.

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Ogata, T., D. Ayusawa, M. Namba, E. Takahashi, M. Oshimura, and M. Oishi. "Chromosome 7 suppresses indefinite division of nontumorigenic immortalized human fibroblast cell lines KMST-6 and SUSM-1." Molecular and Cellular Biology 13, no. 10 (October 1993): 6036–43. http://dx.doi.org/10.1128/mcb.13.10.6036.

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Using nontumorigenic immortalized human cell lines KMST-6 (KMST) and SUSM-1 (SUSM), we attempted to identify the chromosome that carries a putative senescence-related gene(s). These cell lines are the only ones that have been established independently from normal human diploid fibroblasts following in vitro mutagenesis. We first examined restriction fragment length polymorphisms on each chromosome of these immortalized cell lines and their parental cell lines and found specific chromosomal alterations common to these cell lines (a loss of heterozygosity in KMST and a deletion in SUSM) on the long arm of chromosome 7. In addition to these, we also found that introduction of chromosome 7 into these cell lines by means of microcell fusion resulted in the cessation of cell division, giving rise to cells resembling cells in senescence. Introduction of other chromosomes, such as chromosomes 1 and 11, on which losses of heterozygosity were also detected in one of the cell lines (KMST), to either KMST or SUSM cells or of chromosome 7 to several tumor-derived cell lines had no effect on their division potential. These results strongly suggest that a gene(s) affecting limited-division potential or senescence of normal human fibroblasts is located on chromosome 7, probably at the long arm of the chromosome, representing the first case in which a specific chromosome reverses the immortal phenotype of otherwise normal human cell lines.

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Gecheff, K., T. Hvarleva, S. Georgiev, T. Wilkes, and A. Karp. "Cytological and molecular evidence of deletion of ribosomal RNA genes in chromosome 6 of barley (Hordeum vulgare)." Genome 37, no. 3 (June 1, 1994): 419–25. http://dx.doi.org/10.1139/g94-059.

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The barley chromosomal mutant T-35, in which only one pair of satellite chromosomes is apparent, was analyzed using a range of cytological and molecular techniques. Using conventional Feulgen staining, Giemsa and silver banding, in situ hybridization, and Southern blot analysis, unequivocal cytological and molecular evidence was obtained that T-35 is a homozygous deletion of rRNA genes residing in the nucleolus organizer region (NOR) of chromosome 6. According to the criteria of arm ratio and Giemsa-banding pattern of this chromosome, the deletion involved the whole NOR, one of the breakpoints being localized in the short arm proximally to the NOR-associated heterochromatic band, the other probably in the satellite of the chromosome. As a result of this deletion, an increased activity of the rRNA genes (as indicated by the size of the silver bands) on the other NOR-bearing chromosome (chromosome 7) was observed. The possible reasons for this phenomenon are discussed.Key words: barley, nucleolar organizing region, deletion, silver and Giemsa banding, in situ hybridization.

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Atli, Emine Ikbal, Hakan Gurkan, Engin Atli, Ulfet Vatansever, Betul Acunas, and Cisem Mail. "De Novo Subtelomeric 6p25.3 Deletion with Duplication of 6q23.3-q27: Genotype–Phenotype Correlation." Journal of Pediatric Genetics 09, no. 01 (August 12, 2019): 032–39. http://dx.doi.org/10.1055/s-0039-1694703.

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AbstractDuplications of 6q and deletions of 6p have been reported in more than 30 cases of live born infants and given rise to widespread abnormalities recognizable as a specific clinical syndrome. Different phenotypes have been described with variable clinical signs. Most cases involve the coexistence of unbalanced translocations affecting one or the other of the chromosomes. However, duplication of both chromosome 6q and deletion of 6p regions have been reported in only a few cases. Here, we report the first duplication of chromosome band 6q23.3–q27 with deletion of 6p25.3. This is the first case in the literature involving changes to these specific chromosomal regions; a medium size duplication of the distal long arm and smaller deletion of the terminal short arm of chromosome 6. In the literature, there are no other cases where these two specific chromosomal aberrations are observed together. Conventional chromosome analysis was performed to investigate the patient. Chromosome structure was identified using fluorescence in situ hybridization for subtelomeric regions of chromosome 6 and array comparative genomic hybridization analysis (array-CGH).

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Mahesh, G., N. B. Ramachandra, and H. A. Ranganath. "Autoradiographic study of transcription and dosage compensation in the sex and neo-sex chromosome of Drosophila nasuta nasuta and Drosophila nasuta albomicans." Genome 44, no. 1 (February 1, 2001): 71–78. http://dx.doi.org/10.1139/g00-100.

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Cellular autoradiography is used to study the transcription patterns of the polytene X chromosomes in Drosophila nasuta nasuta and D. n. albomicans. D. n. nasuta, with 2n = 8, includes a pair of complete heteromorphic sex chromosomes, whereas D. n. albomicans, with 2n = 6, has a pair of metacentric neo-sex chromosomes representing incomplete heteromorphic sex chromosomes. The neo-X chromosome has two euchromatic arms, one representing the ancestral X while the other represents the ancestral autosome 3 chromosomes. The metacentric neo-Y chromosome has one arm with a complete heterochromatic ancestral Y and the other arm with a euchromatic ancestral autosome 3. The transcription study has revealed that the X chromosome in D. n. nasuta is hyperactive, suggesting complete dosage compensation, while in the neo-X chromosome of D. n. albomicans the ancestral X chromosome is hyperactive and the ancestral autosome 3, which is part of the neo-sex chromosome, is similar to any other autosomes. This finding shows dosage compensation on one arm (XLx/) of the neo-X chromosome, while the other arm (XR3/YR3) is not dosage compensated and has yet to acquire the dosage compensatory mechanism.Key words: Drosophila, chromosomal races, neo-sex chromosome, transcription and dosage compensation.

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Miyashita, Naohiko, Cathy C. Laurie-Ahlberg, Alan N. Wilton, and Ted H. Emigh. "QUANTITATIVE ANALYSIS OF X CHROMOSOME EFFECTS ON THE ACTIVITIES OF THE GLUCOSE 6-PHOSPHATE AND 6-PHOSPHOGLUCONATE DEHYDROGENASES OF DROSOPHILA MELANOGASTER." Genetics 113, no. 2 (June 1, 1986): 321–35. http://dx.doi.org/10.1093/genetics/113.2.321.

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ABSTRACT By combining 20 X chromosomes with five autosomal backgrounds, the relative importance of these factors with respect to the activity variations of G6PD and 6PGD in Drosophila melanogaster were investigated. Analysis of variance revealed that there exist significant X chromosome, autosomal background and genetic interaction effects. The effect of the X chromosome was due mainly to the two allozymic forms of each enzyme, but some within-allozyme effects were also detected. From the estimated variance components, it was concluded that the variation attributed to the autosomal background is much larger than the variation attributed to the X chromosome, even when the effect of the allozymes is included. The segregation of the allozymes seems to account for about 10% of the total activity variation of each enzyme. The variation due to the interaction between the X chromosome and the autosomal background is much smaller than variations attributed either to the X chromosome or to the autosomal background. The interaction effect is indicated by the change of the ranking of the X chromosomes for different autosomal backgrounds. Highly significant and positive correlation between G6PD and 6PGD activities was detected. Again, the contribution of the autosomal background to the correlation was much larger than that attributed to the X chromosome.

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Dissertations / Theses on the topic "Chromosome 6"

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Hammarsund, Marianne. "Genetic changes in lymphoid leukemia /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-628-5841-6/.

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HODGES-GARCIA, YVONNE KATHLEEN. "PURIFICATION AND CHARACTERIZATION OF BACTERIAL PHAGE PHI29 GENE 6 PROTEIN." Diss., The University of Arizona, 1986. http://hdl.handle.net/10150/183864.

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A DNA fragment containing the coding region for gene 6 of Bacterial phage ϕ29 was placed into an expression vector. The ϕ29 gene 6 protein was isolated in large amounts by chromatography on double-stranded DNA cellulose and DE52 cellulose. The ϕ29 gene 6 protein was determined to be greater 95% pure and has a molecular weight of approximately 16,000. The ϕ29 gene 6 protein is thought to be a dimer in its native form. The partial N-terminal amino acid sequence of the purified protein is identically to the inferred amino acid sequence from the nucleotide sequence of ϕ29 gene 6. Gene 6 protein of ϕ29 aggregates in a more purified state which suggest protein to protein interactions. Purified gene 6 protein did not stimulate the ϕ29 in vitro DNA replication system and may require binding with other replication proteins to enable it to function. Gene 6 protein binds weakly to double-stranded and single-strand DNA cellulose. There is segmental amino acid sequence and secondary structure homology with adenovirus DNA binding protein Antibody to gene 6 protein inhibits it from binding to ϕ29 DNA. The results presented in this dissertation suggest that ϕ29 gene 6 protein is a weak DNA bind protein and may not be required for the in vitro ϕ29 DNA replication system.

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Holm, Sofia. "Molecular genetic studies of psoriasis susceptibility in 6p21.3 /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-225-X.

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Kholodnyuk, Irina. "A microcell hybrid based elimination test to identify human chromosome 3 regions that antagonize tumor growth /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-581-6/.

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Calero, Moreno Teresa. "Genetic changes in childhood acute lymphoblastic leukaemia and other lymphoid malignancies /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4625-6/.

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Johonnett, Peter. "Replication timing analysis of the major histocompatibility complex on human chromosome 6." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395158.

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Kabir, Sadia. "Molecular analysis of structure of chromosome 6R of triticale T701-4-6 /." Title page, summary and contents only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phk108.pdf.

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DUGAST, ISABELLE. "Genetique moleculaire de l'hemochromatose idiopathique : etude du gene ferritine h du chromosome 6." Rennes 1, 1988. http://www.theses.fr/1988REN10062.

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Recherche d'une forme nouvelle de ferritine, attribuee au chromosome 6, dans la region du locus hi, marquee par les haplotypes hla. Mise en evidence d'un gene de grande taille dont les coupures enzymatiques suggerent la presence possible d'introns. Ce clone permet de decrire un polymorphisme possible du gene ferritine h sur le chromosome 6

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BLANCHE, HELENE. "Cartographie du chromosome 6 humain, localisation et etude d'homologues du complexe t murin." Paris 6, 1991. http://www.theses.fr/1991PA066421.

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Nous avons construit une carte genetique du bras court du chromosome 6 humain (6p), composee de 17 loci lies les uns aux autres, qui s'etend d'une region proche du telomere jusqu'au centromere. Les marqueurs y sont particulierement denses dans la partie proximale aux trois loci les plus telomeriques, constituant un outil tres utile pour la localisation de genes d'interet. Du fait de l'homologie entre le chromosome 6 humain et le chromosome 17 murin dans la region du complexe t, nous avons localise genetiquement trois homologues humains de genes murins de la partie proximale de ce complexe. Les genes humains, localises vers la region telomerique du bras long du chromosome 6, sont organises de maniere semblable aux homologues murins portes par les haplotypes t murins. Deux homologues humains d'une sequence murine de la partie distale du complexe t, ont ete clones. Un a ete localise genetiquement sur le bras long du chromosome 9. L'autre, exprime dans les testicules, a ete localise, par hybridation in situ et genetiquement, a proximite de la region hla-classe i du cote distal

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Miyagi, Mikiko. "Exploitation of bacterial artificial chromosome (BAC) libraries to enhance the efficiency of genome mapping." Thesis, Queensland University of Technology, 2002. https://eprints.qut.edu.au/37140/6/37140_Digitised%20Thesis.pdf.

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Books on the topic "Chromosome 6"

1

Robin, Cook. Chromosome 6. Paris: Éd. France loisirs, 2001.

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Robin, Cook. Chromosome 6. Thorndike, Me: Thorndike Press, 1997.

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Robin, Cook. Chromosome 6. New York: Putnam, 1997.

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Robin, Cook. Chromosome 6. New York: Berkley Books, 1998.

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Robin, Cook. Chromosome 6. London: Pan, 1997.

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Robin, Cook. Toxin and Chromosome 6. London: Pan, 2004.

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Leake, Mark C., ed. Chromosome Architecture. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2221-6.

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Sobit, R. C., G. Obe, and R. S. Athwal, eds. Some Aspects of Chromosome Structure and Functions. Dordrecht: Springer Netherlands, 2002. http://dx.doi.org/10.1007/978-94-010-0334-6.

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Menasce, Lia Patricia. Deletions of the long arm of chromosome 6 in acute lymphoblastic leukaemia and non-Hodgkin's lymphoma. Manchester: University of Manchester, 1994.

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Jean, Frézal, Klinger Harold P. 1929-, and March of Dimes Birth Defects Foundation., eds. Human gene mapping, 9: Paris Conference (1987), Ninth International Workshop on Human Gene Mapping at the University of Paris, Faculté de Médecine, France, September 6-11, 1987. Basel: Karger, 1987.

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Book chapters on the topic "Chromosome 6"

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Wyandt, Herman E., and Vijay S. Tonk. "Chromosome 6." In Human Chromosome Variation: Heteromorphism and Polymorphism, 83–85. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0896-9_11.

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Nair, Savithri Preetha. "Madras II." In Chromosome Woman, Nomad Scientist, 103–21. London: Routledge India, 2022. http://dx.doi.org/10.4324/9781003267089-6.

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Vergani, Debora. "The Y-Chromosomal STRs in Forensic Genetics: Y Chromosome STRs." In Forensic DNA Analysis, 77–89. Includes bibliographical references and index.: Apple Academic Press, 2020. http://dx.doi.org/10.1201/9781003043027-6.

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Benedetti, Fabrizio, Dusan Racko, Julien Dorier, and Andrzej Stasiak. "Introducing Supercoiling into Models of Chromosome Structure." In Modeling the 3D Conformation of Genomes, 115–38. Boca Raton : Taylor & Francis, 2018. | Series: Series in computational biophysics ; 4: CRC Press, 2019. http://dx.doi.org/10.1201/9781315144009-6.

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Phillips, R. L. "Chromosomal Translocations Involving the Nucleolus Organizer Region or Satellite of Chromosome 6." In The Maize Handbook, 342–45. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4612-2694-9_49.

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Casalone, R., A. Minelli, G. Butti, P. Gaetani, V. Silvani, C. L. Solero, and C. Danesino. "Gene Dosage Effect in Cells with Monosomy of Chromosome 22 Derived from Human Meningiomas." In Proceedings of the 8th European Congress of Neurosurgery, Barcelona, September 6–11, 1987, 114–17. Vienna: Springer Vienna, 1988. http://dx.doi.org/10.1007/978-3-7091-8978-8_24.

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Liu, Guifu, Shaohong Qu, Bo Zhou, Lirong Zeng, and Guo-liang Wang. "Broad-Spectrum Resistance Genes PI2(T) and PI9(T) are Clustered on Chromosome 6." In Rice Blast: Interaction with Rice and Control, 79–86. Dordrecht: Springer Netherlands, 2004. http://dx.doi.org/10.1007/978-0-306-48582-4_10.

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Boehm, B. O., P. Kühnl, C. Rosak, K. Schöffling, W. Spielmann, and S. Seidl. "Segregation analysis and determination of parentship by use of RFLP’s corresponding to genes of the MHC on chromosome 6 and the short arm of chromosome 11." In Advances in Forensic Haemogenetics, 383–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73330-7_73.

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Adachi, Noritaka, Aya Kurosawa, and Hideki Koyama. "Highly Proficient Gene Targeting by Homologous Recombination in the Human Pre-B Cell Line Nalm-6." In Chromosomal Mutagenesis, 17–29. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-232-8_2.

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Vivó, Lorena Rodrigo, Tantra Martínez Benito, and Azarina Ferro Barbero. "Chromosomal Analysis of Sperm." In Handbook of Genetic Diagnostic Technologies in Reproductive Medicine, 51–60. 2nd ed. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003024941-6.

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Conference papers on the topic "Chromosome 6"

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Zheng, Yun-Ling, Xin Zhou, Christopher A. Loffredo, Peter G. Shields, and Bing Sun. "Abstract 3817: Chromosome specific telomeres and breast cancer risk." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3817.

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van Ree, Janine H., Karthik B. Jeganathan, Fang Jin, and Jan M. van Deursen. "Abstract 2992: Mitotic role for Pten in accurate chromosome segregation." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2992.

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Zasadil, Lauren M., Mark Burkard, and Beth A. Weaver. "Abstract 1750: Clinically relevant paclitaxel concentrations cause chromosome missegregation rather than mitotic arrest." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1750.

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Yamada, Hiroshi Y., Yuting Zhang, Wei Dai, and Chinthalapally V. Rao. "Abstract 1752: Consequences of high Chromosome Instability (CIN) in SGO1(Shugoshin1) CIN model mice." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1752.

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Kwong, Lawrence N., and Lynda Chin. "Abstract LB-45: Multiple melanoma suppressors are downregulated by loss of human chromosome 10." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-lb-45.

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Cannon-Albright, Lisa A., Craig C. Teerlink, and Neeraj Agarwal. "Abstract 1341: Identification of significant linkage evidence for lethal prostate cancer on chromosome arm 11p15." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1341.

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Yung, Man Kuen, Chi Wai Yip, Phyllis Fung Yi Cheung, and Siu Tim Cheung. "Abstract 4015: Amplification of GEP at chromosome 17q21 and its overexpression in human liver cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4015.

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Kotoula, Vassiliki, Mattheos Bobos, George Kouvatseas, Christos Papadimitriou, Kyriaki Papadopoulou, Elpida Charalambous, Eleftheria Tsolaki, and George Fountzilas. "Abstract 1918: Genomic CNV testing on chromosome 17q genes reveals clinically relevant subtypes in breast cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1918.

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Hill-Baskin, Anne E., Sabrina H. Spiezio, David DeSantis, Colleen Croniger, John D. Lambris, Joseph H. Nadeau, and Nathan A. Berger. "Abstract 2413: Diet-induced non-alcoholic steatohepatitis and hepatocellular carcinoma in chromosome substitution strains of mice." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2413.

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Fernandez-L, Africa, and Anna M. Kenney. "Abstract 2485: The Hippo downstream effector YAP promotes survival, radiation resistance and chromosome instability in medulloblastoma." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2485.

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Reports on the topic "Chromosome 6"

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Trent, J. M. International workshop on chromosome 6. Final report, June 1, 1992--May 31, 1993. Office of Scientific and Technical Information (OSTI), February 1994. http://dx.doi.org/10.2172/10143657.

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Weller, Joel I., Derek M. Bickhart, Micha Ron, Eyal Seroussi, George Liu, and George R. Wiggans. Determination of actual polymorphisms responsible for economic trait variation in dairy cattle. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600017.bard.

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The project’s general objectives were to determine specific polymorphisms at the DNA level responsible for observed quantitative trait loci (QTLs) and to estimate their effects, frequencies, and selection potential in the Holstein dairy cattle breed. The specific objectives were to (1) localize the causative polymorphisms to small chromosomal segments based on analysis of 52 U.S. Holstein bulls each with at least 100 sons with high-reliability genetic evaluations using the a posteriori granddaughter design; (2) sequence the complete genomes of at least 40 of those bulls to 20 coverage; (3) determine causative polymorphisms based on concordance between the bulls’ genotypes for specific polymorphisms and their status for a QTL; (4) validate putative quantitative trait variants by genotyping a sample of Israeli Holstein cows; and (5) perform gene expression analysis using statistical methodologies, including determination of signatures of selection, based on somatic cells of cows that are homozygous for contrasting quantitative trait variants; and (6) analyze genes with putative quantitative trait variants using data mining techniques. Current methods for genomic evaluation are based on population-wide linkage disequilibrium between markers and actual alleles that affect traits of interest. Those methods have approximately doubled the rate of genetic gain for most traits in the U.S. Holstein population. With determination of causative polymorphisms, increasing the accuracy of genomic evaluations should be possible by including those genotypes as fixed effects in the analysis models. Determination of causative polymorphisms should also yield useful information on gene function and genetic architecture of complex traits. Concordance between QTL genotype as determined by the a posteriori granddaughter design and marker genotype was determined for 30 trait-by-chromosomal segment effects that are segregating in the U.S. Holstein population; a probability of <10²⁰ was used to accept the null hypothesis that no segregating gene within the chromosomal segment was affecting the trait. Genotypes for 83 grandsires and 17,217 sons were determined by either complete sequence or imputation for 3,148,506 polymorphisms across the entire genome. Variant sites were identified from previous studies (such as the 1000 Bull Genomes Project) and from DNA sequencing of bulls unique to this project, which is one of the largest marker variant surveys conducted for the Holstein breed of cattle. Effects for stature on chromosome 11, daughter pregnancy rate on chromosome 18, and protein percentage on chromosome 20 met 3 criteria: (1) complete or nearly complete concordance, (2) nominal significance of the polymorphism effect after correction for all other polymorphisms, and (3) marker coefficient of determination >40% of total multiple-regression coefficient of determination for the 30 polymorphisms with highest concordance. The missense polymorphism Phe279Tyr in GHR at 31,909,478 base pairs on chromosome 20 was confirmed as the causative mutation for fat and protein concentration. For effect on fat percentage, 12 additional missensepolymorphisms on chromosome 14 were found that had nearly complete concordance with the suggested causative polymorphism (missense mutation Ala232Glu in DGAT1). The markers used in routine U.S. genomic evaluations were increased from 60,000 to 80,000 by adding markers for known QTLs and markers detected in BARD and other research projects. Objectives 1 and 2 were completely accomplished, and objective 3 was partially accomplished. Because no new clear-cut causative polymorphisms were discovered, objectives 4 through 6 were not completed.

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Lapidot, Moshe, and Vitaly Citovsky. molecular mechanism for the Tomato yellow leaf curl virus resistance at the ty-5 locus. United States Department of Agriculture, January 2016. http://dx.doi.org/10.32747/2016.7604274.bard.

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Tomato yellow leaf curl virus (TYLCV) is a major pathogen of tomato that causes extensive crop loss worldwide, including the US and Israel. Genetic resistance in the host plant is considered highly effective in the defense against viral infection in the field. Thus, the best way to reduce yield losses due to TYLCV is by breeding tomatoes resistant or tolerant to the virus. To date, only six major TYLCV-resistance loci, termed Ty-1 to Ty-6, have been characterized and mapped to the tomato genome. Among tomato TYLCV-resistant lines containing these loci, we have identified a major recessive quantitative trait locus (QTL) that was mapped to chromosome 4 and designated ty-5. Recently, we identified the gene responsible for the TYLCV resistance at the ty-5 locus as the tomato homolog of the gene encoding messenger RNA surveillance factor Pelota (Pelo). A single amino acid change in the protein is responsible for the resistant phenotype. Pelo is known to participate in the ribosome-recycling phase of protein biosynthesis. Our hypothesis was that the resistant allele of Pelo is a “loss-of-function” mutant, and inhibits or slows-down ribosome recycling. This will negatively affect viral (as well as host-plant) protein synthesis, which may result in slower infection progression. Hence we have proposed the following research objectives: Aim 1: The effect of Pelota on translation of TYLCV proteins: The goal of this objective is to test the effect Pelota may or may not have upon translation of TYLCV proteins following infection of a resistant host. Aim 2: Identify and characterize Pelota cellular localization and interaction with TYLCV proteins: The goal of this objective is to characterize the cellular localization of both Pelota alleles, the TYLCV-resistant and the susceptible allele, to see whether this localization changes following TYLCV infection, and to find out which TYLCV protein interacts with Pelota. Our results demonstrate that upon TYLCV-infection the resistant allele of pelota has a negative effect on viral replication and RNA transcription. It is also shown that pelota interacts with the viral C1 protein, which is the only viral protein essential for TYLCV replication. Following subcellular localization of C1 and Pelota it was found that both protein localize to the same subcellular compartments. This research is innovative and potentially transformative because the role of Peloin plant virus resistance is novel, and understanding its mechanism will lay the foundation for designing new antiviral protection strategies that target translation of viral proteins. BARD Report - Project 4953 Page 2

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Weller, Joel I., Harris A. Lewin, and Micha Ron. Determination of Allele Frequencies for Quantitative Trait Loci in Commercial Animal Populations. United States Department of Agriculture, February 2005. http://dx.doi.org/10.32747/2005.7586473.bard.

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Individual loci affecting economic traits in dairy cattle (ETL) have been detected via linkage to genetic markers by application of the granddaughter design in the US population and the daughter design in the Israeli population. From these analyses it is not possible to determine allelic frequencies in the population at large, or whether the same alleles are segregating in different families. We proposed to answer this question by application of the "modified granddaughter design", in which granddaughters with a common maternal grandsire are both genotyped and analyzed for the economic traits. The objectives of the proposal were: 1) to fine map three segregating ETL previously detected by a daughter design analysis of the Israeli dairy cattle population; 2) to determine the effects of ETL alleles in different families relative to the population mean; 3) for each ETL, to determine the number of alleles and allele frequencies. The ETL on Bostaurusautosome (BT A) 6 chiefly affecting protein concentration was localized to a 4 cM chromosomal segment centered on the microsatellite BM143 by the daughter design. The modified granddaughter design was applied to a single family. The frequency of the allele increasing protein percent was estimated at 0.63+0.06. The hypothesis of equal allelic frequencies was rejected at p<0.05. Segregation of this ETL in the Israeli population was confirmed. The genes IBSP, SPP1, and LAP3 located adjacent to BM143 in the whole genome cattle- human comparative map were used as anchors for the human genome sequence and bovine BAC clones. Fifteen genes within 2 cM upstream of BM143 were located in the orthologous syntenic groups on HSA4q22 and HSA4p15. Only a single gene, SLIT2, was located within 2 cM downstream of BM143 in the orthologous HSA4p15 region. The order of these genes, as derived from physical mapping of BAC end sequences, was identical to the order within the orthologous syntenic groups on HSA4: FAM13A1, HERC3. CEB1, FLJ20637, PP2C-like, ABCG2, PKD2. SPP, MEP, IBSP, LAP3, EG1. KIAA1276, HCAPG, MLR1, BM143, and SLIT2. Four hundred and twenty AI bulls with genetic evaluations were genotyped for 12 SNPs identified in 10 of these genes, and for BM143. Seven SNPs displayed highly significant linkage disequilibrium effects on protein percentage (P<0.000l) with the greatest effect for SPP1. None of SNP genotypes for two sires heterozygous for the ETL, and six sires homozygous for the ETL completely corresponded to the causative mutation. The expression of SPP 1 and ABCG2 in the mammary gland corresponded to the lactation curve, as determined by microarray and QPCR assays, but not in the liver. Anti-sense SPP1 transgenic mice displayed abnormal mammary gland differentiation and milk secretion. Thus SPP 1 is a prime candidate gene for this ETL. We confirmed that DGAT1 is the ETL segregating on BTA 14 that chiefly effects fat concentration, and that the polymorphism is due to a missense mutation in an exon. Four hundred Israeli Holstein bulls were genotyped for this polymorphism, and the change in allelic frequency over the last 20 years was monitored.

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