Academic literature on the topic 'Patched Gene'
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Journal articles on the topic "Patched Gene"
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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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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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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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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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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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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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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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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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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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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.
Full textDissertations / Theses on the topic "Patched Gene"
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Rahnama, Fahimeh. "Molecular complexities of patched signaling in cancer development /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-897-1/.
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Hidalgo-Downing, Alicia. "Molecular cloning of patched and analysis of its role in intrasegmental patterning in D. melanogaster." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.258158.
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Undén, Anne Birgitte. "Studies on basal cell carcinoma with emphasis on the role of the human homologue of the drosophila patched gene /." Stockholm, 1997. http://diss.kib.ki.se/1997/91-628-2788-X.
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de, Zwaan Sally Elizabeth. "The Genetics of Basal Cell Carcinoma of the Skin." Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/3878.
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BCC is the commonest cancer in European-derived populations and Australia has the highest recorded incidence in the world, creating enormous individual and societal cost in management of this disease. The incidence of this cancer has been increasing internationally, with evidence of a 1 to 2% rise in incidence in Australia per year over the last two decades. The main four epidemiological risk factors for the development of BCC are ultraviolet radiation (UVR) exposure, increasing age, male sex, and inability to tan. The pattern and timing of UVR exposure is important to BCC risk, with childhood and intermittent UVR exposure both associated with an increased risk. The complex of inherited characteristics making up an individual’s ‘sun sensitivity’ is also important in determining BCC risk. Very little is known about population genetic susceptibility to BCC outside of the rare genodermatosis Gorlin syndrome. Mutations in the tumour suppressor gene patched (PTCH) are responsible for this BCC predisposition syndrome and the molecular pathway and target genes of this highly conserved pathway are well described. Derangments in this pathway occur in sporadic BCC development, and the PTCH gene is an obvious candidate to contribute to non-syndromic susceptibility to BCC. The melanocortin 1 receptor (MC1R) locus is known to be involved in pigmentary traits and the cutaneous response to UVR, and variants have been associated with skin cancer risk. Many other genes have been considered with respect to population BCC risk and include p53, HPV, GSTs, and HLAs. There is preliminary evidence for specific familial aggregation of BCC, but very little known about the causes. 56 individuals who developed BCC under the age of 40 in the year 2000 were recruited from the Skin and Cancer Foundation of Australia’s database. This represents the youngest 7 – 8% of Australians with BCC from a database that captures approximately 10% of Sydney’s BCCs. 212 of their first degree relatives were also recruited, including 89 parents and 123 siblings of these 56 probands. All subjects were interviewed with respect to their cancer history and all reports of cancer verified with histopathological reports where possible. The oldest unaffected sibling for each proband (where available) was designated as an intra-family control. All cases and control siblings filled out a questionnaire regarding their pigmentary and sun sensitivity factors and underwent a skin examination by a trained examiner. Peripheral blood was collected from these cases and controls for genotyping of PTCH. All the exons of PTCH for which mutations have been documented in Gorlin patients were amplified using PCR. PCR products were screened for mutations using dHPLC, and all detectable variants sequenced. Prevalence of BCC and SCC for the Australian population was estimated from incidence data using a novel statistical approach. Familial aggregation of BCC, SCC and MM occurred within the 56 families studied here. The majority of families with aggregation of skin cancer had a combination of SCC and BCC, however nearly one fifth of families in this study had aggregation of BCC to the exclusion of SCC or MM, suggesting that BCCspecific risk factors are also likely to be at work. Skin cancer risks for first-degree relatives of people with early onset BCC were calculated: sisters and mothers of people with early-onset BCC had a 2-fold increased risk of BCC; brothers had a 5-fold increased risk of BCC; and sisters and fathers of people with early-onset BCC had over four times the prevalence of SCC than that expected. For melanoma, the increased risk was significant for male relatives only, with a 10-fold increased risk for brothers of people with early-onset BCC and 3-fold for fathers. On skin examination of cases and controls, several phenotypic factors were significantly associated with BCC risk. These included increasing risk of BCC with having fair, easyburning skin (ie decreasing skin phototype), and with having signs of cumulative sun damage to the skin in the form of actinic keratoses. Signs reflecting the combination of pigmentary characteristics and sun exposure - in the form of arm freckling and solar lentigines - also gave subjects a significantly increased risk BCC. Constitutive red-green reflectance of the skin was associated with decreased risk of BCC, as measured by spectrophotometery. Other non-significant trends were seen that may become significant in larger studies including associations of BCC with propensity to burn, moderate tanning ability and an inability to tan. No convincing trend for risk of BCC was seen with the pigmentary variables of hair or eye colour, and a non-significant reduced risk of BCC was associated with increasing numbers of seborrhoeic keratoses. Twenty PTCH exons (exons 2, 3, 5 to 18, and 20 to 23) were screened, accounting for 97% of the coding regions with published mutations in PTCH. Nine of these 20 exons were found to harbour single nucleotide polymorphisms (SNPs), seen on dHPLC as variant melting curves and confirmed on direct sequencing. SNPs frequencies were not significantly different to published population frequencies, or to Australian general population frequencies where SNP database population data was unavailable. Assuming a Poisson distribution, and having observed no mutations in a sample of 56, we can be 97.5% confident that if there are any PTCH mutations contributing to early-onset BCC in the Australian population, then their prevalence is less than 5.1%. Overall, this study provides evidence that familial aggregation of BCC is occurring, that first-degree relatives are at increased risk of all three types of skin cancer, and that a combination of environmental and genetic risk factors are likely to be responsible. The PTCH gene is excluded as a major cause of this increased susceptibility to BCC in particular and skin cancer in general. The weaknesses of the study design are explored, the possible clinical relevance of the data is examined, and future directions for research into the genetics of basal cell carcinoma are discussed.
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de, Zwaan Sally Elizabeth. "The Genetics of Basal Cell Carcinoma of the Skin." University of Sydney, 2008. http://hdl.handle.net/2123/3878.
Full textAbstract:
Doctor of Philosophy(PhD)BCC is the commonest cancer in European-derived populations and Australia has the highest recorded incidence in the world, creating enormous individual and societal cost in management of this disease. The incidence of this cancer has been increasing internationally, with evidence of a 1 to 2% rise in incidence in Australia per year over the last two decades. The main four epidemiological risk factors for the development of BCC are ultraviolet radiation (UVR) exposure, increasing age, male sex, and inability to tan. The pattern and timing of UVR exposure is important to BCC risk, with childhood and intermittent UVR exposure both associated with an increased risk. The complex of inherited characteristics making up an individual’s ‘sun sensitivity’ is also important in determining BCC risk. Very little is known about population genetic susceptibility to BCC outside of the rare genodermatosis Gorlin syndrome. Mutations in the tumour suppressor gene patched (PTCH) are responsible for this BCC predisposition syndrome and the molecular pathway and target genes of this highly conserved pathway are well described. Derangments in this pathway occur in sporadic BCC development, and the PTCH gene is an obvious candidate to contribute to non-syndromic susceptibility to BCC. The melanocortin 1 receptor (MC1R) locus is known to be involved in pigmentary traits and the cutaneous response to UVR, and variants have been associated with skin cancer risk. Many other genes have been considered with respect to population BCC risk and include p53, HPV, GSTs, and HLAs. There is preliminary evidence for specific familial aggregation of BCC, but very little known about the causes. 56 individuals who developed BCC under the age of 40 in the year 2000 were recruited from the Skin and Cancer Foundation of Australia’s database. This represents the youngest 7 – 8% of Australians with BCC from a database that captures approximately 10% of Sydney’s BCCs. 212 of their first degree relatives were also recruited, including 89 parents and 123 siblings of these 56 probands. All subjects were interviewed with respect to their cancer history and all reports of cancer verified with histopathological reports where possible. The oldest unaffected sibling for each proband (where available) was designated as an intra-family control. All cases and control siblings filled out a questionnaire regarding their pigmentary and sun sensitivity factors and underwent a skin examination by a trained examiner. Peripheral blood was collected from these cases and controls for genotyping of PTCH. All the exons of PTCH for which mutations have been documented in Gorlin patients were amplified using PCR. PCR products were screened for mutations using dHPLC, and all detectable variants sequenced. Prevalence of BCC and SCC for the Australian population was estimated from incidence data using a novel statistical approach. Familial aggregation of BCC, SCC and MM occurred within the 56 families studied here. The majority of families with aggregation of skin cancer had a combination of SCC and BCC, however nearly one fifth of families in this study had aggregation of BCC to the exclusion of SCC or MM, suggesting that BCCspecific risk factors are also likely to be at work. Skin cancer risks for first-degree relatives of people with early onset BCC were calculated: sisters and mothers of people with early-onset BCC had a 2-fold increased risk of BCC; brothers had a 5-fold increased risk of BCC; and sisters and fathers of people with early-onset BCC had over four times the prevalence of SCC than that expected. For melanoma, the increased risk was significant for male relatives only, with a 10-fold increased risk for brothers of people with early-onset BCC and 3-fold for fathers. On skin examination of cases and controls, several phenotypic factors were significantly associated with BCC risk. These included increasing risk of BCC with having fair, easyburning skin (ie decreasing skin phototype), and with having signs of cumulative sun damage to the skin in the form of actinic keratoses. Signs reflecting the combination of pigmentary characteristics and sun exposure - in the form of arm freckling and solar lentigines - also gave subjects a significantly increased risk BCC. Constitutive red-green reflectance of the skin was associated with decreased risk of BCC, as measured by spectrophotometery. Other non-significant trends were seen that may become significant in larger studies including associations of BCC with propensity to burn, moderate tanning ability and an inability to tan. No convincing trend for risk of BCC was seen with the pigmentary variables of hair or eye colour, and a non-significant reduced risk of BCC was associated with increasing numbers of seborrhoeic keratoses. Twenty PTCH exons (exons 2, 3, 5 to 18, and 20 to 23) were screened, accounting for 97% of the coding regions with published mutations in PTCH. Nine of these 20 exons were found to harbour single nucleotide polymorphisms (SNPs), seen on dHPLC as variant melting curves and confirmed on direct sequencing. SNPs frequencies were not significantly different to published population frequencies, or to Australian general population frequencies where SNP database population data was unavailable. Assuming a Poisson distribution, and having observed no mutations in a sample of 56, we can be 97.5% confident that if there are any PTCH mutations contributing to early-onset BCC in the Australian population, then their prevalence is less than 5.1%. Overall, this study provides evidence that familial aggregation of BCC is occurring, that first-degree relatives are at increased risk of all three types of skin cancer, and that a combination of environmental and genetic risk factors are likely to be responsible. The PTCH gene is excluded as a major cause of this increased susceptibility to BCC in particular and skin cancer in general. The weaknesses of the study design are explored, the possible clinical relevance of the data is examined, and future directions for research into the genetics of basal cell carcinoma are discussed.
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Daniels, Graeme P. "Characterisation of the Musca domestica (Diptera) homologue of the Drosophila melanogaster segment polarity gene patched, and the cloning of a cDNA fragment, PD, from Acheta domesticus." Thesis, University of Edinburgh, 1998. http://hdl.handle.net/1842/13559.
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The Drosophila segment polarity gene, patched (ptc), encodes a transmembrane protein that is the receptor for the hedgehog intercellular signalling molecule. Mutations in the human ptc gene, have been shown to be responsible for Gorlin's syndrome and a predisposition to nevoid basal cell carcinomas. In this study, partial clones of patched homologues were isolated from the long germ band developing house fly, Musca domestica (Diptera), and the intermediate germ band developing house cricket, Acheta domesticus (Orthoptera). Sequence data obtained from the Musca domestica clones showed a high degree of similarity with the Drosophila ptc gene sequence, indicating that the Musca domestica clones contain real ptc homologues. The Acheta ptc fragment was cloned using degenerate PCR, and sequence data has shown it has a high degree of similarity to the comparable regions of other ptc homologues. Two phagemid clones were also isolated from an Acheta cDNA library using a strategy designed to isolate Acheta ptc. One of these clones, PD, was used to create RNA in situ hybridization probes, and its expression was examined during Acheta embryogenesis, although it was later shown that PD was not an Acheta ptc homologue. Expression of the Musca ptc homologue was examined during early development using RNA in situ hybridisation, and immunohistochemistry. These studies have shown that the expression of ptc during Musca domestica development is very similar to ptc expression patterns seen during the early development of Drosophila, suggesting that ptc may be fulfilling a similar role in both species.
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Diniz, Marina Goncalves. "Estudo das múltiplas isoformas do gene Patched1 em ceratocisto odontogênico." Universidade Federal de Minas Gerais, 2008. http://hdl.handle.net/1843/BUOS-9TDFHF.
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O ceratocisto odontogênico (CO) é uma neoplasia benigna que possui um comportamento biológico agressivo. O CO está associado a alterações no gene homologo 1 ao gene patched de Drosophila (PTCH1). Este gene possui diversas isoformas geradas pelo uso alternativo do primeiro exon (1b, 1d e 1e). As isoformas podem possuir diferenças na sua expressão, na capacidade de agir como receptor da proteína sinalizadora Hedgehog (Hh) e na inibição da própria via. Levando em consideração que a via Hh pode estar envolvida na patogênese do CO, o objetivo deste estudo foi avaliar a presença dos diferentes RNAm do gene PTCH1 nesta lesão. Foram incluídos no estudo 40 CO, sendo 12 esporádicos e 28 associados à Síndrome do Carcinoma Basocelular nevóide (SCBN). Destas lesões, 17 eram primárias, 17 eram marsupializadas e 6 eram recorrentes. O estudo da expressão dos exons 1 alternativos do gene PTCH1 foi realizado através da técnica da Transcriptase Reversa PCR (RT PCR). Os resultados demonstram que 90% dos CO, esporádicos e associados à SCBN, expressam o transcrito 1b enquanto nenhum folículo dentário (controle) apresenta a expressão desta isoforma. O RNAm do 1d é expresso na maioria dos CO e em todos os controles. Foi detectada a expressão do transcrito 1b em todas as lesões primárias, porém isso não ocorreu em 4 (24%) lesões marsupializadas. O perfil de expressão dos transcritos na mucosa adjacente à lesão é semelhante ao do CO. Concluímos que a via Hh está superativada no CO e na mucosa adjacente e que a marsupialização pode alterar a expressão das isoformas.
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Poon, Hiu-ching. "A study of the regulatory roles of Hedgehog in the enteric nervous system development by the conditional knockout of Patched1 enteric gene in the enteric neural crest cells." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B42841604.
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Cordeiro, Erick M. G. "Patterns of infestation, dispersion, and gene flow in Rhyzopertha dominica based on population genetics and ecological modeling." Diss., Kansas State University, 2016. http://hdl.handle.net/2097/32642.
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Doctor of PhilosophyDepartment of Entomology
James F. Campbell
Thomas W. Phillips
Movement is a fundamental feature of animals that impacts processes across multiple scales in space and time. Due to the heterogeneous and fragmented nature of habitats that make up landscapes, movement is not expected to be random in all instances, and an increase in fitness is an expected consequence for those that can optimize movement to find valuable and scarce recourses. I studied the movement of Rhyzopertha dominica (Coleoptera: Bostrichidae), one of the most important pests of stored grain worldwide, within and between resource patches. At a fine spatial scale, I identified factors that contribute to overall and upward movement in the grain mass. Three-week-old insects tented to stay closer to the surface than one or two-week-old insects. Females tended to be more active and to explore more than males. I also found that males tended to stay closer to the surface than females and that might be related to the ability to attract females from outside the patch since there was no significant difference regarding female’s attraction within the grain patch. Interaction with feeding sites or other individuals of the same sex creates positive feedback and a more clumped spatial pattern of feeding and foraging behavior. On the other hand, interaction with individuals of different sex creates negative feedback and a more random or overdispersed pattern. At a broad spatial scale, I studied the long-term consequence of R. dominica movement on the development of population structure within the U.S. To evaluate population structure, I used reduced representation of the genome followed by direct sequencing of beetles collected from different locations across the U.S where wheat or rice is produced and stored. Ecoregions were more important in explaining structure of R. dominica populations than crop type. I also found significant isolation by distance; however, model selection primarily elected grain production and movement variables to explain population differentiation and diversity. Understanding animal movement is essential to establishing relationships between distribution and surrounding landscape, and this knowledge can improve conservation and management strategies.
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Liang, Guihua. "K⁺ channels in the inner ear : electrophysiological and molecular studies /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7349-971-4/.
Full textBooks on the topic "Patched Gene"
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Shrewsbury, Stephen. Defy Your DNA: How the New Gene Patch Personalized Medicines Will Help You Overcome Your Greatest Health Challenges. 10 Finger Press, 2013.
Find full textBook chapters on the topic "Patched Gene"
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Weinstein, P. D., P. A. Schweitzer, A. George, and J. J. Cebra. "Expression of heavy chain genes is restricted in Peyer’s patch germinal center B cells." In Advances in Mucosal Immunology, 302–5. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1848-1_85.
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Lemtiri-Chlieh, Fouad, and Rashid Ali. "Characterization of Heterologously Expressed Transporter Genes by Patch- and Voltage-Clamp Methods: Application to Cyclic Nucleotide-Dependent Responses." In Cyclic Nucleotide Signaling in Plants, 67–93. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-441-8_6.
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Allendorf, Fred W., W. Chris Funk, Sally N. Aitken, Margaret Byrne, and Gordon Luikart. "Population Connectivity." In Conservation and the Genomics of Populations, 425–50. Oxford University Press, 2022. http://dx.doi.org/10.1093/oso/9780198856566.003.0019.
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We discuss the roles of gene flow, genetic drift, and selection in determining the distribution of genetic variation in complex, real-world landscapes. A metapopulation is a group of populations that experience some degree of gene flow among them. Metapopulation structure can have complex effects on patterns of genetic variation within and among populations. For species that do not naturally occur in discrete habitat patches, a landscape genetics framework is more appropriate. Landscape genetics combines population genetics, landscape ecology, and spatial statistics to understand how environmental heterogeneity affects gene flow and genetic variation. Habitat loss and fragmentation have severed connectivity among populations of many formerly continuous species, isolating populations that then lose genetic variation due to reduced gene flow. Genetic rescue, the supplementation of small inbred populations with immigrants from larger more genetically diverse populations, can be used to increase genetic diversity and reduce extinction probabilities of populations isolated by habitat fragmentation.
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Levitan, Irwin B., and Leonard K. Kaczmarek. "Diversity in the Structure and Function of Ion Channels." In The Neuron, 127–50. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199773893.003.0007.
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Voltage clamp and patch clamp techniques are used to reveal heterogeneity of ion currents carried through voltage-dependent sodium, calcium, and potassium channels. Advances in channel molecular biology have made it clear that the diversity of ion channels is even greater than was suspected from these electrophysiological measurements. This diversity is achieved by several different mechanisms, including the existence of multiple genes for the pore-forming α subunits of ion channels, alternative splicing of the messenger RNA transcribed from each individual gene, formation of heterotetramers containing different α subunits of potassium channels, and modulation of channel properties by auxiliary subunits that may themselves comprise a large and diverse family of proteins. Moreover, potassium channels can be further categorized into voltage-dependent, calcium-dependent, sodium-dependent, two-pore, and inward rectifier channels. Emerging evidence suggests that many human diseases are associated with dysfunction of individual classes of ion channels in neurons.
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Fain, Gordon L. "The senses." In Sensory Transduction, 1–17. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198835028.003.0001.
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“The senses” is the introductory chapter of the book Sensory Transduction and describes early studies in the anatomy of sense organs and physiology of the senses. It introduces methods in physiology and molecular biology, which were critical tools used to unlock the secrets of sensation, including intracellular and extracellular recording, patch-clamp recording, gene cloning and expression, and structural studies such as cryo-EM. It concludes by describing in detail the discovery of the piezo proteins, which are the stretch-sensitive channels now known to be responsible for much of mammalian touch and proprioception.
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London, Bette. "Material Boys." In Posthumous Lives, 33–71. Cornell University Press, 2022. http://dx.doi.org/10.7591/cornell/9781501762352.003.0002.
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This chapter discusses the material culture of World War I, focusing on the objects of commemorative biography—the memorial volumes, collected, curated, and often privately published, that became familiar relics in so many mourning households. It considers both the materials that went into these volumes, including the soldiers' own writings, and the volumes themselves as material objects. The chapter therefore differs in its methodology from a strictly literary reading of the text but also from a strictly materialist one of the artifact. Patched together out of scraps and fragments—letters and poems by the deceased; memoirs by family members; tributes from others; snippets of inspirational literature; photographs and drawings; diary fragments—these commemorative volumes deploy a proliferation of materials to make up for lives that lacked recognizable fullness and dimension. In doing so, these volumes created a new kind of biographical hybrid, occupying an ambiguous place between text and object and an ambiguous place in a rapidly changing genre.
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Yeh, Hermes, Stavros Therianos, and Shao-Ming Lu. "Combining Patch-Clamp Recording and Gene Profiling in Single Neurons." In Methods in Alcohol-Related Neuroscience Research. CRC Press, 2002. http://dx.doi.org/10.1201/9781420042092.ch4.
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Thompson, Daniel B. "Different Spatial Scales of Natural Selection and Gene Flow: The Evolution of Behavioral Geographic Variation and Phenotypic Plasticity." In Geographic Variation in Behavior. Oxford University Press, 1999. http://dx.doi.org/10.1093/oso/9780195082951.003.0006.
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The environmental variables hypothesized to cause behavioral adaptation are distributed across a wide array of spatial scales, from local variation in factors such as food sources and territorial encounters to regional or continental variation in factors such as seasonality and the presence of predators. Geographic variation in behavior, the topic of this book, is just one of the potential evolutionary responses to environmental variation. Because behavioral divergence among populations generated by disparate natural selection can be counterbalanced by the homogenizing influence of gene flow, adaptive geographic variation can evolve only if the spatial scale of variation in natural selection is greater than the scale of gene flow (Endler 1977, Slatkin 1978). If geographic variation does not evolve because the spatial scale of selection is smaller than the scale of gene flow, populations may instead evolve adaptive phenotypic plasticity (Bradshaw 1965); the expression, by a single genotype, of different fitness-enhancing phenotypes in different environments. Because the same evolutionary processes operating on different spatial scales can generate behavioral geographic variation, behavioral phenotypic plasticity, or geographic variation in phenotypic plasticity, I devote this chapter to development of a hierarchical perspective tor studying environmental variation and behavioral evolution. This perspective emphasizes the shared evolutionary processes and research methodologies common to different levels of spatial variation, such as the balance of gene flow, natural selection, and genetic drift, the relationship between environmental patch size and local adaptation, and the effects of historical contingencies and genetic constraints on behavioral adaptation and phenotypic plasticity. In what follows, I review behavioral research in two unrelated taxa to illustrate the range of possible evolutionary responses to different patterns of environmental variation. First, I discuss different spatial scales of adaptation in the climbing behavior of deer mice (Peromyscus maniculatus) and provide a hierarchical analysis of the effects of natural selection, genetic drift, and gene flow. Second, I discuss diet-induced phenotypic plasticity in the feeding behavior of acridid grasshoppers (Melanoplus femurrubrum and M. sanguinipes) and the evolution of behavioral norms of reaction in response to local spatial and temporal variation in plant environments.
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"Community Ecology of Stream Fishes: Concepts, Approaches, and Techniques." In Community Ecology of Stream Fishes: Concepts, Approaches, and Techniques, edited by William J. Matthews. American Fisheries Society, 2010. http://dx.doi.org/10.47886/9781934874141.ch1.
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<em>Abstract</em>.— In 1985, at the annual meeting of the American Society of Ichthyologists and Herpetologists in Knoxville, Tennessee, the symposium “Community and Evolutionary Ecology of North American Stream Fishes,” organized by W. J. Matthews and D. C. Heins, resulted in the 1987 publication of a 30-paper volume. Main themes included conceptual models of life history, zoogeography, or community dynamics; habitat use; responses to stress or to flooding; predator effects; effects of grazing fishes; ecomorphology, morphological plasticity, niche packing, or rarity; anthropogenic changes in fish faunas; life history variation or tactics; and genetic variation or divergence. Numerous papers from that symposium were influential on future research in stream fish ecology. As of 1985, many approaches or techniques now in common use did not exist or were barely used by stream fish ecologists, including gene sequencing, geographic information systems, the Internet, “landscape ecology,” “metapopulations,” “macroecology,” and “riverscapes,” and global warming was not yet a household word. Since the 1985 symposium, there have been two important international meetings of fish ecologists in Spain, organized by Javier Lobon-Cervia. The current volume compliments these efforts by attempting to synthesize advances in the field of stream fish community ecology. Since the 1985 symposium, fish ecologists have adopted many new approaches, including more large-scale and long-term surveys, stable isotopes, and ecological stoichiometry, among others, and linkages among habitat patches, fish effects in stream ecosystems, and effects of climate change are a major focus. This volume from the 2008 symposium includes 24 papers that document progress in stream fish ecology since the 1985 symposium, some of which take new theoretical and empirical approaches to address questions that were unasked or unanswerable two decades ago.
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"Correlation of Ion Channel Activity with Gene Expression Using Single-Cell RT-PCR and Patch-Clamp Techniques." In Ion Channels in the Pulmonary Vasculature, 690–701. CRC Press, 2005. http://dx.doi.org/10.1201/b14190-35.
Full textConference papers on the topic "Patched Gene"
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Ramalingam, Naveen, Long-Qing Chen, Xin-Hao Yang, Liqun Deng, Qing-Hui Wang, Eric Yap Peng Huat, Chiew Hoon Neo, and Hai-Qing Gong. "A Surface-Directed Microfluidic Scheme for Parallel Nanoliter PCR Array Suitable for Point-of-Care Testing." In ASME 2009 7th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2009. http://dx.doi.org/10.1115/icnmm2009-82052.
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In resource-limited settings, it is impractical to get access to a diagnostic laboratory having sophisticated instruments, and it is desirable to use disposable point-of-care diagnostic chips that do not require liquid handling or pumping instruments for sample distribution among an array of reactors. In addition to the pump-less sample loading method, the challenge to seal an array of reactors without the use of microvalves or mechanical parts still persists. Implementation of microvalve array adds complexity to the chip fabrication and operation processes, and also reduces the space on the microchip. In this paper, we report the development of a high-throughput quantitative PCR chip platform for parallel analyses of multiple gene targets. The PCR mixture distribution among an array of 80 microreactors and subsequent isolation of the reactors were solely realized by a two-step surface tension-based microfluidic scheme, which eliminates the use of pumps, valves and liquid handling instruments. Confinement of the PCR mixture inside the micro reactors was achieved by implementing hybrid flow-restriction passive valves. The microreactors were isolated from each other by the flow of a curable liquid sealant delivered through microchannels by capillary action. We also investigated the effect of detergents that are present in most commercial PCR buffers. Presence of detergents makes the PCR buffer much more wetting on the passive capillary valve surface and this imposes another challenge to the design of the conventional hydrophobic patch valves which has been successfully used for deionized water. We demonstrated a successful capillary valve array with a common air venting channel having a hydrophobic surface for restricting the flow of PCR buffer containing surfactant. The interconnected microreactor array was fabricated on a glass chip substrate with approximate volume of 250 nl microreactor volume for PCR. A different set of PCR primers were preloaded into different microreactor on the PCR array chip for simultaneous amplification of multiple genes. Fluorescent signals from all the microreactors were simultaneously detected at every PCR thermal cycle using EvaGreen fluorescent dye on an in-house real-time PCR instrument. The capability of the scalable PCR array chip was demonstrated by amplifying a fragment of uidA gene for beta-glucuronidase of E. coli genome. Key technical issues related to chip operation such as PCR inhibition on the acid-washed glass substrate, and PCR compatibility of the sealant in both the uncured and cured states have been addressed.
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Chiu, Chun-Chia, Jeng-Lin Li, Yu-Fen Wang, Bor-Sheng Ko, and Chi-Chun Lee. "A Coarse-to-Fine Pathology Patch Selection for Improving Gene Mutation Prediction in Acute Myeloid Leukemia." In 2022 44th Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2022. http://dx.doi.org/10.1109/embc48229.2022.9871814.
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Huitema, L., J. L. Valdes, H. Wong, and A. Crunteanu. "Optical Switching of GeTe Phase Change Material: Application to a Frequency Agile Millimeter-Waves Patch Antenna." In 12th European Conference on Antennas and Propagation (EuCAP 2018). Institution of Engineering and Technology, 2018. http://dx.doi.org/10.1049/cp.2018.0888.
Full textReports on the topic "Patched Gene"
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Montville, Thomas J., and Roni Shapira. Molecular Engineering of Pediocin A to Establish Structure/Function Relationships for Mechanistic Control of Foodborne Pathogens. United States Department of Agriculture, August 1993. http://dx.doi.org/10.32747/1993.7568088.bard.
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This project relates the structure of the bacteriocin molecule (which is genetically determined) to its antimicrobial function. We have sequenced the 19,542 bp pediocin plasmid pMD136 and developed a genetic transfer system for pediococci. The pediocin A operon is complex, containing putative structural, immunity, processing, and transport genes. The deduced sequence of the pediocin A molecule contains 44 amino acids and has a predicted PI of 9.45. Mechanistic studies compared the interaction of pediocin PA-1 and nisin with Listeria monocytgenes cells and model lipid systems. While significant nisin-induced intracellular ATP depletion is caused by efflux, pediocin-induced depletion is caused exclusively by hydrolysis. Liposomes derived from L. monocytogenes phospholipids were used to study the physical chemistry of pediocin and nisin interactions with lipids. Their different pH optima are the results of different specific ionizable amino acids. We generated a predicted 3-D structural model for pediocin PA-1 and used a variety of mutant pediocins to demonstrate that the "positive patch" at residues 11 and 12 (and not the YGNGV consensus sequence) is responsible for the binding step of pediocin action. This structure/function understanding gained here provides necessary prerequisites to the more efficacious use of bacteriocins to control foodborne pathogens.