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Journal articles on the topic 'Patched Gene'

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Published: 4 June 2021

Last updated: 20 February 2023

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1

Ellis, Tammy, Ian Smyth, Emily Riley, Scott Graham, Kate Elliot, Monica Narang, Graham F. Kay, Carol Wicking, and Brandon Wainwright. "Patched 1 conditional null allele in mice." genesis 36, no. 3 (July 2003): 158–61. http://dx.doi.org/10.1002/gene.10208.

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2

Phillips, R. G., I. J. Roberts, P. W. Ingham, and J. R. Whittle. "The Drosophila segment polarity gene patched is involved in a position-signalling mechanism in imaginal discs." Development 110, no. 1 (September 1, 1990): 105–14. http://dx.doi.org/10.1242/dev.110.1.105.

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We demonstrate the role of the segment polarity gene patched (ptc) in patterning in the cuticle of the adult fly. Genetic mosaics of a lethal allele of patched show that the contribution of patched varies in a position-specific manner, defining three regions in the wing where ptc clones, respectively, behave as wild-type cells, affect vein formation, or are rarely recovered. Analysis of twin clones demonstrates that the reduced clone frequency results from a proliferation failure or cell loss. In the region where clones upset venation, they autonomously fail to form veins and also non-autonomously induce ectopic veins in adjacent wild-type cells. In heteroallelic combinations with lethal alleles, two viable alleles produce distinct phenotypes: (1) loss of structures and mirror-image duplications in the region where patched clones fail to proliferate; (2) vein abnormalities in the anterior compartment. We propose that these differences reflect independently mutable functions within the gene. We show the pattern of patched transcription in the developing imaginal wing disc in relation to the expression of certain other reporter genes using a novel double-labelling method combining non-radioactive detection of in situ hybridization with beta-galactosidase detection. The patched transcript is present throughout the anterior compartment, with a stripe of maximal intensity along the A/P compartment border extending into the posterior compartment. We propose that the patched product is a component of a cell-to-cell position-signalling mechanism, a proposal consistent with the predicted structure of the patched protein.

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3

Ingham, Philip W. "The patched gene in development and cancer." Current Opinion in Genetics & Development 8, no. 1 (February 1998): 88–94. http://dx.doi.org/10.1016/s0959-437x(98)80067-1.

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4

Ingham, Philip W. "The patched gene in development and cancer." Current Opinion in Genetics & Development 8, no. 3 (June 1998): 371. http://dx.doi.org/10.1016/s0959-437x(98)80096-8.

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5

Hidalgo, A., and P. Ingham. "Cell patterning in the Drosophila segment: spatial regulation of the segment polarity gene patched." Development 110, no. 1 (September 1, 1990): 291–301. http://dx.doi.org/10.1242/dev.110.1.291.

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Intrasegmental patterning in the Drosophila embryo requires the activity of the segment polarity genes. The acquisition of positional information by cells during embryogenesis is reflected in the dynamic patterns of expression of several of these genes. In the case of patched, early ubiquitous expression is followed by its repression in the anterior portion of each parasegment; subsequently each broad band of expression splits into two narrow stripes. In this study we analyse the contribution of other segment polarity gene functions to the evolution of this pattern; we find that the first step in patched regulation is under the control of engrailed whereas the second requires the activity of both cubitus interruptusD and patched itself. Furthermore, the products of engrailed, wingless and hedgehog are essential for maintaining the normal pattern of expression of patched.

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6

Marigo, V., M. P. Scott, R. L. Johnson, L. V. Goodrich, and C. J. Tabin. "Conservation in hedgehog signaling: induction of a chicken patched homolog by Sonic hedgehog in the developing limb." Development 122, no. 4 (April 1, 1996): 1225–33. http://dx.doi.org/10.1242/dev.122.4.1225.

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Hedgehog genes have been implicated in inductive signaling during development in a variety of organisms. A key element of the hedgehog signaling system is encoded by the gene patched. In Drosophila hedgehog regulates gene expression by antagonizing the action of patched. In addition, patched is itself a transcriptional target of hedgehog signaling. We have isolated a chicken patched homolog and find it to be strongly expressed adjacent to all tissues where members of the hedgehog family are expressed. As in Drosophila, ectopic expression of Sonic hedgehog leads to ectopic induction of chicken Patched. Based on this regulatory conservation, vertebrate Patched is likely to be directly downstream of Sonic hedgehog signaling. An important role of Sonic hedgehog is the regulation of anterior/posterior pattern in the developing limb bud. Since Patched is directly downstream of the hedgehog signal, the extent of high level Patched expression provides a measure of the distance that Sonic hedgehog diffuses and directly acts. On this basis, we find that Sonic hedgehog directly acts as a signal over only the posterior third of the limb bud. During limb patterning, secondary signals are secreted in both the mesoderm (e.g. Bone Morphogenetic Protein-2) and apical ectodermal ridge (e.g. Fibroblast Growth Factor-4) in response to Sonic hedgehog. Thus knowing which is the direct target tissue is essential for unraveling the molecular patterning of the limb. The expression of Patched provides a strong indication that the mesoderm and not the ectoderm is the direct target of Sonic hedgehog signaling in the limb bud. Finally we demonstrate that induction of Patched requires Sonic hedgehog but, unlike Bone Morphogenetic Protein-2 and Hox genes, does not require Fibroblast Growth Factor as a co-inducer. It is therefore a more direct target of Sonic hedgehog than previously reported patterning genes.

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7

Concordet, J. P., K. E. Lewis, J. W. Moore, L. V. Goodrich, R. L. Johnson, M. P. Scott, and P. W. Ingham. "Spatial regulation of a zebrafish patched homologue reflects the roles of sonic hedgehog and protein kinase A in neural tube and somite patterning." Development 122, no. 9 (September 1, 1996): 2835–46. http://dx.doi.org/10.1242/dev.122.9.2835.

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Signalling by members of the Hedgehog family of secreted proteins plays a central role in the development of vertebrate and invertebrate embryos. In Drosophila, transduction of the Hedgehog signal is intimately associated with the activity of protein kinase A and the product of the segment polarity gene patched. We have cloned a homologue of patched from the zebrafish Danio rerio and analysed the spatiotemporal regulation of its transcription during embryonic development in both wild-type and mutant animals. We find a striking correlation between the accumulation of patched1 transcripts and cells responding to sonic hedgehog activity both in the neurectoderm and mesoderm, suggesting that like its Drosophila counterpart, patched1 is regulated by sonic hedgehog activity. Consistent with this interpretation, mis-expression of sonic hedgehog results in ectopic activation of patched1 transcription. Using dominant negative and constitutively active forms of the protein kinase A subunits, we also show that expression of patched1 as well as of other sonic hedgehog targets, is regulated by protein kinase A activity. Taken together, our findings suggest that the mechanism of signalling by Hedgehog family proteins has been highly conserved during evolution.

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8

Capdevila, J., F. Pariente, J. Sampedro, J. L. Alonso, and I. Guerrero. "Subcellular localization of the segment polarity protein patched suggests an interaction with the wingless reception complex in Drosophila embryos." Development 120, no. 4 (April 1, 1994): 987–98. http://dx.doi.org/10.1242/dev.120.4.987.

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The product of the segment polarity gene patched is a transmembrane protein involved in the cell communication processes that establish polarity within the embryonic segments of Drosophila. Monoclonal antibodies have been raised against the patched protein, and by immunoelectron microscopy part of the patched staining is found associated with discrete regions of the lateral plasma membrane of the embryonic epidermal cells. Using a mutation affecting endocytosis (shibire) we find that patched is a membrane-bound protein, which is internalized by endocytosis, and that the preferential sites of accumulation resemble the described localization of the cell-cell adhesive junctions of the epidermal cells. patched partially co-localizes with the wingless protein in the wingless-expressing and nearby cells, in structures that seem to be endocytic vesicles. These data suggest the interaction of patched protein with elements of the reception complex of wingless, as a way to control the wingless expression.

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9

Ingham, P. W., A. M. Taylor, and Y. Nakano. "Role of the Drosophila patched gene in positional signalling." Nature 353, no. 6340 (September 1991): 184–87. http://dx.doi.org/10.1038/353184a0.

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10

Takabatake, Takashi, Masanori Ogawa, Tadashi C. Takahashi, Makoto Mizuno, Mitsumasa Okamoto, and Kazuhito Takeshima. "Hedgehog and patched gene expression in adult ocular tissues." FEBS Letters 410, no. 2-3 (June 30, 1997): 485–89. http://dx.doi.org/10.1016/s0014-5793(97)00645-5.

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11

Gemmill, Robert M., James D. West, Ferenc Boldog, Naotake Tanaka, Linda J. Robinson, David I. Smith, Frederick Li, and Harry A. Drabkin. "The hereditary renal cell carcinoma 3;8 translocation fuses FHIT to a patched-related gene, TRC8." Proceedings of the National Academy of Sciences 95, no. 16 (August 4, 1998): 9572–77. http://dx.doi.org/10.1073/pnas.95.16.9572.

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The 3;8 chromosomal translocation, t(3;8)(p14.2;q24.1), was described in a family with classical features of hereditary renal cell carcinoma. Previous studies demonstrated that the 3p14.2 breakpoint interrupts the fragile histidine triad gene (FHIT) in its 5′ noncoding region. However, evidence that FHIT is causally related to renal or other malignancies is controversial. We now show that the 8q24.1 breakpoint region encodes a 664-aa multiple membrane spanning protein, TRC8, with similarity to the hereditary basal cell carcinoma/segment polarity gene, patched. This similarity involves two regions of patched, the putative sterol-sensing domain and the second extracellular loop that participates in the binding of sonic hedgehog. In the 3;8 translocation, TRC8 is fused to FHIT and is disrupted within the sterol-sensing domain. In contrast, the FHIT coding region is maintained and expressed. In a series of sporadic renal carcinomas, an acquired TRC8 mutation was identified. By analogy to patched, TRC8 might function as a signaling receptor and other pathway members, to be defined, are mutation candidates in malignant diseases involving the kidney and thyroid.

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12

Nakatomi, M., I. Morita, K. Eto, and M. S. Ota. "Sonic Hedgehog Signaling is Important in Tooth Root Development." Journal of Dental Research 85, no. 5 (May 2006): 427–31. http://dx.doi.org/10.1177/154405910608500506.

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Hertwig’s epithelial root sheath (HERS) is important for tooth root formation, but the molecular basis for the signaling of root development remains uncertain. We hypothesized that Sonic hedgehog (Shh) signaling is involved in the HERS function, because it mediates epithelial-mesenchymal interactions during embryonic odontogenesis. We examined the gene expression patterns of Shh signaling in murine developing molar roots. Shh and Patched2 transcripts were identified in the HERS, whereas Patched1, Smoothened, and Gli1 were expressed in the proliferative dental mesenchyme in addition to the HERS. To confirm whether Shh signaling physiologically functions in vivo, we analyzed mesenchymal dysplasia ( mes) mice carrying an abnormal C-terminus of the PATCHED1 protein. In the mutant, cell proliferation was repressed around the HERS at 1 wk. Moreover, the molar eruption was disturbed, and all roots were shorter than those in control littermates at 4 wks. These results indicate that Shh signaling is important in tooth root development. Abbreviations used: BrdU, 5-bromo-2′-deoxyuridine; HERS, Hertwig’s epithelial root sheath; NFI-C/CTF, nuclear factor Ic/CAAT box transcription factor; PCNA, proliferating cell nuclear antigen; Ptc, patched; Shh, sonic hedgehog; Smo, smoothened.

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13

Nagano, T., M. Ueda, and M. Ichihashi. "062 Expression of human patched gene in various skin neoplasms." Journal of Dermatological Science 15, no. 2 (August 1997): 113. http://dx.doi.org/10.1016/s0923-1811(97)81765-3.

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14

Yan, Taiqiang, Mark Angelini, Benjamin A. Alman, Irene L. Andrulis, and Jay S. Wunder. "PATCHED-ONE or SMOOTHENED Gene Mutations Are Infrequent in Chondrosarcoma." Clinical Orthopaedics and Related Research 466, no. 9 (June 10, 2008): 2184–89. http://dx.doi.org/10.1007/s11999-008-0332-2.

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15

Goodrich, L. V., R. L. Johnson, L. Milenkovic, J. A. McMahon, and M. P. Scott. "Conservation of the hedgehog/patched signaling pathway from flies to mice: induction of a mouse patched gene by Hedgehog." Genes & Development 10, no. 3 (February 1, 1996): 301–12. http://dx.doi.org/10.1101/gad.10.3.301.

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16

Hiltunen, Mimmu K., Alex J. Timmis, Maren Thomsen, Danai S. Gkotsi, Hideo Iwaï, Orquidea M. Ribeiro, Adrian Goldman, and Natalia A. Riobo-Del Galdo. "PTCHD1 Binds Cholesterol but Not Sonic Hedgehog, Suggesting a Distinct Cellular Function." International Journal of Molecular Sciences 24, no. 3 (January 31, 2023): 2682. http://dx.doi.org/10.3390/ijms24032682.

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Deleterious mutations in the X-linked Patched domain-containing 1 (PTCHD1) gene may account for up to 1% of autism cases. Despite this, the PTCHD1 protein remains poorly understood. Structural similarities to Patched family proteins point to a role in sterol transport, but this hypothesis has not been verified experimentally. Additionally, PTCHD1 has been suggested to be involved in Hedgehog signalling, but thus far, the experimental results have been conflicting. To enable a variety of biochemical and structural experiments, we developed a method for expressing PTCHD1 in Spodoptera frugiperda cells, solubilising it in glycol-diosgenin, and purifying it to homogeneity. In vitro and in silico experiments show that PTCHD1 function is not interchangeable with Patched 1 (PTCH1) in canonical Hedgehog signalling, since it does not repress Smoothened in Ptch1−/− mouse embryonic fibroblasts and does not bind Sonic Hedgehog. However, we found that PTCHD1 binds cholesterol similarly to PTCH1. Furthermore, we identified 13 PTCHD1-specific protein interactors through co-immunoprecipitation and demonstrated a link to cell stress responses and RNA stress granule formation. Thus, our results support the notion that despite structural similarities to other Patched family proteins, PTCHD1 may have a distinct cellular function.

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17

Lam, Ching-Wan, Chi-Yan Leung, Kam-Cheong Lee, Jingwu Xie, Fai-Man Lo, Tak-Shing Au, Sui-Fan Tong, Miu-Kuen Poon, Loi-Yuen Chan, and Nai-Ming Luk. "Novel mutations in the PATCHED gene in basal cell nevus syndrome." Molecular Genetics and Metabolism 76, no. 1 (May 2002): 57–61. http://dx.doi.org/10.1016/s1096-7192(02)00021-5.

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18

Bejsovec, A., and E. Wieschaus. "Segment polarity gene interactions modulate epidermal patterning in Drosophila embryos." Development 119, no. 2 (October 1, 1993): 501–17. http://dx.doi.org/10.1242/dev.119.2.501.

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Each segment of a Drosophila larva shows a precisely organized pattern of cuticular structures, indicating diverse cellular identities in the underlying epidermis. Mutations in the segment polarity genes alter the cuticle pattern secreted by the epidermal cells; these mutant patterns provide clues about the role that each gene product plays in the development of wild-type epidermal pattern. We have analyzed embryos that are multiply mutant for five key patterning genes: wingless, patched, engrailed, naked and hedgehog. Our results indicate that wild-type activity of these five segment polarity genes can account for most of the ventral pattern elements and that their gene products interact extensively to specify the diverse cellular identities within the epidermis. Two pattern elements can be correlated with individual gene action: wingless is required for formation of naked cuticle and engrailed is required for formation of the first row of denticles in each abdominal denticle belt. The remaining cell types can be produced by different combinations of the five gene activities. wingless activity generates the diversity of cell types within the segment, but each specific cell identity depends on the activity of patched, engrailed, naked and hedgehog. These molecules modulate the distribution and interpretation of wingless signalling activity in the ventral epidermal cells and, in addition, each can contribute to pattern through a pathway independent of the wingless signalling pathway.

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19

Kim, Juhan, Jake J. Flood, Michael R. Kristofich, Cyrus Gidfar, Andrew B. Morgenthaler, Tobias Fuhrer, Uwe Sauer, et al. "Hidden resources in the Escherichia coli genome restore PLP synthesis and robust growth after deletion of the essential gene pdxB." Proceedings of the National Academy of Sciences 116, no. 48 (November 11, 2019): 24164–73. http://dx.doi.org/10.1073/pnas.1915569116.

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PdxB (erythronate 4-phosphate dehydrogenase) is expected to be required for synthesis of the essential cofactor pyridoxal 5′-phosphate (PLP) in Escherichia coli. Surprisingly, incubation of the ∆pdxB strain in medium containing glucose as a sole carbon source for 10 d resulted in visible turbidity, suggesting that PLP is being produced by some alternative pathway. Continued evolution of parallel lineages for 110 to 150 generations produced several strains that grow robustly in glucose. We identified a 4-step bypass pathway patched together from promiscuous enzymes that restores PLP synthesis in strain JK1. None of the mutations in JK1 occurs in a gene encoding an enzyme in the new pathway. Two mutations indirectly enhance the ability of SerA (3-phosphoglycerate dehydrogenase) to perform a new function in the bypass pathway. Another disrupts a gene encoding a PLP phosphatase, thus preserving PLP levels. These results demonstrate that a functional pathway can be patched together from promiscuous enzymes in the proteome, even without mutations in the genes encoding those enzymes.

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20

Stone, Donna M., Mary Hynes, Mark Armanini, Todd A. Swanson, Qimin Gu, Ronald L. Johnson, Matthew P. Scott, et al. "The tumour-suppressor gene patched encodes a candidate receptor for Sonic hedgehog." Nature 384, no. 6605 (November 1996): 129–34. http://dx.doi.org/10.1038/384129a0.

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21

Sampedro, Javier, and Isabel Guerrero. "Unrestricted expression of the Drosophila gene patched allows a normal segment polarity." Nature 353, no. 6340 (September 1991): 187–90. http://dx.doi.org/10.1038/353187a0.

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22

Ling, Gao, Afshin Ahmadian, Åsa Persson, Anne Birgitte Undén, Gijs Afink, Cecilia Williams, Mathias Uhlén, Rune Toftgård, Joakim Lundeberg, and Fredrik Pontén. "PATCHED and p53 gene alterations in sporadic and hereditary basal cell cancer." Oncogene 20, no. 53 (November 2001): 7770–78. http://dx.doi.org/10.1038/sj.onc.1204946.

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23

Cajaiba, Mariana M., Allen E. Bale, Mayra Alvarez-Franco, Joseph McNamara, and Miguel Reyes-Múgica. "Rhabdomyosarcoma, Wilms tumor, and deletion of the patched gene in Gorlin syndrome." Nature Clinical Practice Oncology 3, no. 10 (October 2006): 575–80. http://dx.doi.org/10.1038/ncponc0608.

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24

Kitano, Hisataka, Yuu Koyama, Masamichi Komiya, Naoyuki Sato, and Tomohiro Nakayama. "Basal cell nevus syndrome: New mutation of the patched homologue 1 gene." Journal of Oral and Maxillofacial Surgery, Medicine, and Pathology 26, no. 4 (October 2014): 506–10. http://dx.doi.org/10.1016/j.ajoms.2013.04.016.

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25

Motoyama, Jun, Takashi Takabatake, Kazuhito Takeshima, and Chi-chung Hui. "Ptch2, a second mouse Patched gene is co-expressed with Sonic hedgehog." Nature Genetics 18, no. 2 (February 1998): 104–6. http://dx.doi.org/10.1038/ng0298-104.

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26

Yan, Taiqiang, Mark Angelini, Benjamin A. Alman, Irene L. Andrulis, and Jay S. Wunder. "Erratum to: PATCHED-ONE or SMOOTHENED Gene Mutations Are Infrequent in Chondrosarcoma." Clinical Orthopaedics and Related Research® 467, no. 12 (October 22, 2009): 3356. http://dx.doi.org/10.1007/s11999-009-1134-x.

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27

Capdevila, J., M. P. Estrada, E. Sánchez-Herrero, and I. Guerrero. "The Drosophila segment polarity gene patched interacts with decapentaplegic in wing development." EMBO Journal 13, no. 1 (January 1994): 71–82. http://dx.doi.org/10.1002/j.1460-2075.1994.tb06236.x.

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28

Reinders, Marie G., Antonius F. van Hout, Betûl Cosgun, Aimée D. Paulussen, Edward M. Leter, Peter M. Steijlen, Klara Mosterd, Michel van Geel, and Johan J. Gille. "New mutations and an updated database for the patched-1 (PTCH1 ) gene." Molecular Genetics & Genomic Medicine 6, no. 3 (March 25, 2018): 409–15. http://dx.doi.org/10.1002/mgg3.380.

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29

Bale, Sherri J., Roni T. Falk, and Geraldine R. Rogers. "Patching Together the Genetics of Gorlin Syndrome." Journal of Cutaneous Medicine and Surgery 3, no. 1 (July 1998): 31–34. http://dx.doi.org/10.1177/120347549800300109.

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Background: Gorlin syndrome is an autosomal dominant disorder characterized by developmental defects and susceptibility to cancer, especially to basal cell carcinomas. The genetic basis of this disorder has recently been elucidated. Methods: In this article previous studies are reviewed in which loss of heterozygosity analysis of tumours and normal tissue pointed to a region on chromosome 9 as being involved in Gorlin syndrome. In this light, Knudson's two-hit model is discussed. The identification of the involvement of the patched gene in Gorlin syndrome is reviewed. New data on genotype-phenotype correlations in the syndrome are presented. Results: Loss-of-heterozygosity studies, together with standard family studies using linkage analysis, have proved useful in identifying the location of a gene with complex phenotypic expression. Conclusion: The application of the two-hit model, as utilized in loss-of-heterozygosity studies, has been very useful in elucidating the genetic basis of Gorlin syndrome. There may be a correlation between certain aspects of the mutations in patched and the clinical presentation of the disorder in families.

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30

Johnson, R. L., A. L. Rothman, J. Xie, L. V. Goodrich, J. W. Bare, J. M. Bonifas, A. G. Quinn, et al. "Human Homolog of patched, a Candidate Gene for the Basal Cell Nevus Syndrome." Science 272, no. 5268 (June 14, 1996): 1668–71. http://dx.doi.org/10.1126/science.272.5268.1668.

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31

Pritchard, Joel I., and James M. Olson. "Methylation of PTCH1, the Patched-1 gene, in a panel of primary medulloblastomas." Cancer Genetics and Cytogenetics 180, no. 1 (January 2008): 47–50. http://dx.doi.org/10.1016/j.cancergencyto.2007.09.008.

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32

Fan, Jun, Hiroto Akabane, Xuehai Zheng, Xuan Zhou, Li Zhang, Qiang Liu, Yong-Lian Zhang, Jing Yang, and Guo-Zhang Zhu. "Male germ cell-specific expression of a novel Patched-domain containing gene Ptchd3." Biochemical and Biophysical Research Communications 363, no. 3 (November 2007): 757–61. http://dx.doi.org/10.1016/j.bbrc.2007.09.047.

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33

Hooper, Joan E., and Matthew P. Scott. "The Drosophila patched gene encodes a putative membrane protein required for segmental patterning." Cell 59, no. 4 (November 1989): 751–65. http://dx.doi.org/10.1016/0092-8674(89)90021-4.

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34

Barreto, D. C., A. E. Bale, L. De Marco, and R. S. Gomez. "Immunolocalization of PTCH Protein in Odontogenic Cysts and Tumors." Journal of Dental Research 81, no. 11 (November 2002): 757–60. http://dx.doi.org/10.1177/0810757.

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The human patched gene ( PTCH) functions in both embryologic development and tumor suppression. PTCH mutations have been found in odontogenic keratocysts. However, the expression and localization of the protein product of the gene have not been determined in odontogenic tumors and cysts. We investigated 68 odontogenic lesions by immunohistochemistry, and compared their PTCH expression with that in basal cell carcinomas. All odontogenic lesions, including two keratocysts with truncating mutations, were positive for PTCH. Different types of lesions had different amounts of staining. Lack of staining was noted in the majority of basal cell carcinomas. Taken together, these data suggest that odontogenic keratocysts arise with heterozygous mutations of the PTCH gene.

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35

Bokor, P., and S. DiNardo. "The roles of hedgehog, wingless and lines in patterning the dorsal epidermis in Drosophila." Development 122, no. 4 (April 1, 1996): 1083–92. http://dx.doi.org/10.1242/dev.122.4.1083.

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Rows of cells that flank the parasegment boundary make up a signaling center within the epidermis of the Drosophila embryo. Signals emanating from these cells, encoded by hedgehog (hh) and wingless (wg), are shown to be required for all segment pattern dorsally. Wg activity is required for the differentiation of one cell type, constituting half the parasegment. The gene lines appears to act in parallel to the Wg pathway in the elaboration of this cell type. Hh activity is responsible for three other cell types in the parasegment. Some cell types are specified as Hh activity and interfere with the function of patched, analogous to patterning of imaginal discs. However, some pattern is independent of the antagonism of patched by Hh, and relies instead on novel interactions with lines. Lastly, we provide evidence that decapentaplegic does not mediate patterning by Hh in the dorsal epidermis.

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36

Brailey, L. L., T. Davis, S. E. Kolker, T. C. Murry, D. Thomas, A. E. Bale, and S. M. Ruhoy. "Congenital linear unilateral basal cell nevus: a case report with patched gene molecular studies." Journal of Cutaneous Pathology 34, no. 1 (January 2007): 65–70. http://dx.doi.org/10.1111/j.1600-0560.2006.00580.x.

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37

Dean, Michael. "Towards a unified model of tumor suppression: lessons learned from the human patched gene." Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 1332, no. 2 (April 1997): M43—M52. http://dx.doi.org/10.1016/s0304-419x(96)00043-1.

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38

Kagey, Jacob D., Jordan A. Brown, and Kenneth H. Moberg. "Regulation of Yorkie activity in Drosophila imaginal discs by the Hedgehog receptor gene patched." Mechanisms of Development 129, no. 9-12 (September 2012): 339–49. http://dx.doi.org/10.1016/j.mod.2012.05.007.

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39

Maesawa, Chihaya, Gen Tamura, Takeshi Iwaya, Satoshi Ogasawara, Kaoru Ishida, Nobuhiro Sato, Satoshi Nishizuka, et al. "Mutations in the human homologue of theDrosophila patched gene in esophageal squamous cell carcinoma." Genes, Chromosomes and Cancer 21, no. 3 (March 1998): 276–79. http://dx.doi.org/10.1002/(sici)1098-2264(199803)21:3<276::aid-gcc15>3.0.co;2-n.

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40

Matos, Jefferson David Melo de, Leonardo Jiro Nomura Nakano, Pedro Jacy Santos Diamantino, Guilherme da Rocha Scalzer Lopes, Marco Antonio Bottino, John Eversong Lucena de Vasconcelos, Nathália de Carvalho Ramos, and Valdir Cabral Andrade. "Gorlin-Goltz syndrome: systemic and maxillofacial characteristics." ARCHIVES OF HEALTH INVESTIGATION 10, no. 1 (October 22, 2020): 49–54. http://dx.doi.org/10.21270/archi.v10i1.4853.

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Gorlin-Goltz Syndrome, also known as Nevoid Basal Cell Carcinoma Syndrome, is a rare genetic disorder characterized by the presence of multiple keratocysts in the jaw and basal cell carcinomas, at young age, of palmar and/or plantar depressions, of calcification of the sickle cerebral and skeletal malformations. This syndrome is caused by a mutation of the PTCH1 (patched homolog 1 from Drosophila) gene, a tumor suppressor gene. In this work, the systemic and maxillofacial characteristics of the Gorlin-Goltz syndrome, as well as some neurological, dermatological, musculoskeletal and endocrine alterations, are reviewed. In addition, a case report was added for the purpose of support this study.

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Matos, Jefferson David Melo de, Leonardo Jiro Nomura Nakano, Pedro Jacy Santos Diamantino, Guilherme da Rocha Scalzer Lopes, Marco Antonio Bottino, John Eversong Lucena de Vasconcelos, Nathália de Carvalho Ramos, and Valdir Cabral Andrade. "Gorlin-Goltz syndrome: systemic and maxillofacial characteristics." ARCHIVES OF HEALTH INVESTIGATION 10, no. 1 (October 22, 2020): 49–54. http://dx.doi.org/10.21270/archi.v10i1.4853.

Full text

Abstract:

Gorlin-Goltz Syndrome, also known as Nevoid Basal Cell Carcinoma Syndrome, is a rare genetic disorder characterized by the presence of multiple keratocysts in the jaw and basal cell carcinomas, at young age, of palmar and/or plantar depressions, of calcification of the sickle cerebral and skeletal malformations. This syndrome is caused by a mutation of the PTCH1 (patched homolog 1 from Drosophila) gene, a tumor suppressor gene. In this work, the systemic and maxillofacial characteristics of the Gorlin-Goltz syndrome, as well as some neurological, dermatological, musculoskeletal and endocrine alterations, are reviewed. In addition, a case report was added for the purpose of support this study.

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Shao, Jianguo, Ling Zhang, Jun Gao, Zhaoshen Li, and Zhirong Chen. "Aberrant Expression of PTCH (Patched Gene) and Smo (Smoothened Gene) in Human Pancreatic Cancerous Tissues and Its Association With Hyperglycemia." Pancreas 33, no. 1 (July 2006): 38–44. http://dx.doi.org/10.1097/01.mpa.0000222319.59360.21.

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Laimer, M., K. Önder, P. Schlager, C. M. Lanschuetzer, M. Emberger, S. Selhofer, H. Hintner, and J. W. Bauer. "Nonsense-associated altered splicing of the Patched gene fails to suppress carcinogenesis in Gorlin syndrome." British Journal of Dermatology 159, no. 1 (July 2008): 222–27. http://dx.doi.org/10.1111/j.1365-2133.2008.08617.x.

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BODAK, N. "High mutation frequency of the patched gene in basal cell carcinomas from xeroderma pigmentosum patients." Journal of the European Academy of Dermatology and Venereology 11 (September 1998): S304. http://dx.doi.org/10.1016/s0926-9959(98)95747-6.

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Bodak, N., S. Queille, M. F. Avril, B. Bouadjar, C. Drougard, A. Sarasin, and L. Daya-Grosjean. "High levels of patched gene mutations in basal-cell carcinomas from patients with xeroderma pigmentosum." Proceedings of the National Academy of Sciences 96, no. 9 (April 27, 1999): 5117–22. http://dx.doi.org/10.1073/pnas.96.9.5117.

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Hasenpusch-Theil, Kerstin, Veronique Bataille, Jaana Laehdetie, Franz Obermayr, Julian R. Sampson, and Anna-Maria Frischauf. "Gorlin syndrome: Identification of 4 novel germ-line mutations of the human patched (PTCH) gene." Human Mutation 11, no. 6 (1998): 480. http://dx.doi.org/10.1002/(sici)1098-1004(1998)11:6<480::aid-humu9>3.0.co;2-4.

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Gallet, A., C. Angelats, S. Kerridge, and P. P. Therond. "Cubitus interruptus-independent transduction of the Hedgehog signal in Drosophila." Development 127, no. 24 (December 15, 2000): 5509–22. http://dx.doi.org/10.1242/dev.127.24.5509.

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The Hedgehog (Hh) family of secreted proteins are key factors that control pattern formation in invertebrates and vertebrates. The manner in which Hh molecules regulate a target cell remains poorly understood. In the Drosophila embryo, Hh is produced in identical stripes of cells in the posterior compartment of each segment. From these cells a Hh signal acts in both anterior and posterior directions. In the anterior cells, the target genes wingless and patched are activated whereas posterior cells respond to Hh by expressing rhomboid and patched. Here, we have examined the role of the transcription factor Cubitus interruptus (Ci) in this process. So far, Ci has been thought to be the most downstream component of the Hh pathway capable of activating all Hh functions. However, our current study of a null ci allele, indicates that it is actually not required for all Hh functions. Whereas Hh and Ci are both required for patched expression, the target genes wingless and rhomboid have unequal requirements for Hh and Ci activity. Hh is required for the maintenance of wingless expression before embryonic stage 11 whereas Ci is necessary only later during stage 11. For rhomboid expression Hh is required positively whereas Ci exhibits negative input. These results indicate that factors other than Ci are necessary for Hh target gene regulation. We present evidence that the zinc-finger protein Teashirt is one candidate for this activity. We show that it is required positively for rhomboid expression and that Teashirt and Ci act in a partially redundant manner before stage 11 to maintain wingless expression in the trunk.

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Jain, Neha, Ajay K. Pillai, Nisha Mishra, MD Ishtiyak, G. V. Reddy, and Saksham Nahar. "Gorlin Goltz Syndrome: A Disease in Disguise." Clinical Research and Clinical Trials 5, no. 3 (February 25, 2022): 01–05. http://dx.doi.org/10.31579/2693-4779/080.

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Gorlin Goltz syndrome also known as nevoid basal cell carcinoma is an autosomal dominant inherited disorder caused due to mutation in patched (PTCH) tumor suppressor gene present in the 9q chromosome. Gorlin goltz syndrome display diversified odontogenic as well as systemic manifestations. Early diagnosis and prompt treatment is mandatory to decrease morbidity and mortality. Here we present a subtle case report of a 17-year-old boy who presented with multiple odontogenic keratocysts of the mandible and maxilla which upon further examination was diagnosed as Gorlin Goltz Syndrome.

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Lewis, M. T., S. Ross, P. A. Strickland, C. W. Sugnet, E. Jimenez, M. P. Scott, and C. W. Daniel. "Defects in mouse mammary gland development caused by conditional haploinsufficiency of Patched-1." Development 126, no. 22 (November 15, 1999): 5181–93. http://dx.doi.org/10.1242/dev.126.22.5181.

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In vertebrates, the hedgehog family of cell signaling proteins and associated downstream network components play an essential role in mediating tissue interactions during development and organogenesis. Loss-of-function or misexpression mutation of hedgehog network components can cause birth defects, skin cancer and other tumors. The mammary gland is a specialized skin derivative requiring epithelial-epithelial and epithelial-stromal tissue interactions similar to those required for development of other organs, where these interactions are often controlled by hedgehog signaling. We have investigated the role of the Patched-1 (Ptc1) hedgehog receptor gene in mammary development and neoplasia. Haploinsufficiency at the Ptc1 locus results in severe histological defects in ductal structure, and minor morphological changes in terminal end buds in heterozygous postpubescent virgin animals. Defects are mainly ductal hyperplasias and dysplasias characterized by multilayered ductal walls and dissociated cells impacting ductal lumens. This phenotype is 100% penetrant. Remarkably, defects are reverted during late pregnancy and lactation but return upon involution and gland remodeling. Whole mammary gland transplants into athymic mice demonstrates that the observed dysplasias reflect an intrisic developmental defect within the gland. However, Ptc1-induced epithelial dysplasias are not stable upon transplantation into a wild-type epithelium-free fat pad, suggesting stromal (or epithelial and stromal) function of Ptc1. Mammary expression of Ptc1 mRNA is both epithelial and stromal and is developmentally regulated. Phenotypic reversion correlates with developmentally regulated and enhanced expression of Indian hedgehog (Ihh) during pregnancy and lactation. Data demonstrate a critical mammary role for at least one component of the hedgehog signaling network and suggest that Ihh is the primary hedgehog gene active in the gland.

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Nieuwenhuis, Erica, Jun Motoyama, Paul C. Barnfield, Yoshiaki Yoshikawa, Xiaoyun Zhang, Rong Mo, Michael A. Crackower, and Chi-chung Hui. "Mice with a Targeted Mutation of Patched2 Are Viable but Develop Alopecia and Epidermal Hyperplasia." Molecular and Cellular Biology 26, no. 17 (September 1, 2006): 6609–22. http://dx.doi.org/10.1128/mcb.00295-06.

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ABSTRACT Hedgehog (Hh) signaling plays pivotal roles in tissue patterning and development in Drosophila melanogaster and vertebrates. The Patched1 (Ptc1) gene, encoding the Hh receptor, is mutated in nevoid basal cell carcinoma syndrome, a human genetic disorder associated with developmental abnormalities and increased incidences of basal cell carcinoma (BCC) and medulloblastoma (MB). Ptc1 mutations also occur in sporadic forms of BCC and MB. Mutational studies with mice have verified that Ptc1 is a tumor suppressor. We previously identified a second mammalian Patched gene, Ptc2, and demonstrated its distinct expression pattern during embryogenesis, suggesting a unique role in development. Most notably, Ptc2 is expressed in an overlapping pattern with Shh in the epidermal compartment of developing hair follicles and is highly expressed in the developing limb bud, cerebellum, and testis. Here, we describe the generation and phenotypic analysis of Ptc2 tm1/tm1 mice. Our molecular analysis suggests that Ptc2 tm1 likely represents a hypomorphic allele. Despite the dynamic expression of Ptc2 during embryogenesis, Ptc2 tm1/tm1 mice are viable, fertile, and apparently normal. Interestingly, adult Ptc2 tm1/tm1 male animals develop skin lesions consisting of alopecia, ulceration, and epidermal hyperplasia. While functional compensation by Ptc1 might account for the lack of a strong mutant phenotype in Ptc2-deficient mice, our results suggest that normal Ptc2 function is required for adult skin homeostasis.

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