Готові списки джерел за темами / Gene patterning

Добірка наукової літератури з теми "Gene patterning"

Автор: Grafiati
Опубліковано: 6 липня 2024

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Статті в журналах з теми "Gene patterning":

1

Kala, A., P. K. Jain, and S. H. Friedman. "Patterning of cells through patterning of biology." Mol. BioSyst. 10, no. 7 (2014): 1689–92. http://dx.doi.org/10.1039/c3mb70587k.

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For the first time, patterns of cells have been constructed by spatially manipulating native gene expression. This control of expression was effected using light activated RNA interference (LARI), a technique in which knockdown of gene expression is modulated through siRNA modified with light cleavable groups.
2

Pyrowolakis, George, Ville Veikkolainen, Nir Yakoby, and Stanislav Y. Shvartsman. "Gene regulation during Drosophila eggshell patterning." Proceedings of the National Academy of Sciences 114, no. 23 (June 5, 2017): 5808–13. http://dx.doi.org/10.1073/pnas.1610619114.

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A common path to the formation of complex 3D structures starts with an epithelial sheet that is patterned by inductive cues that control the spatiotemporal activities of transcription factors. These activities are then interpreted by the cis-regulatory regions of the genes involved in cell differentiation and tissue morphogenesis. Although this general strategy has been documented in multiple developmental contexts, the range of experimental models in which each of the steps can be examined in detail and evaluated in its effect on the final structure remains very limited. Studies of the Drosophila eggshell patterning provide unique insights into the multiscale mechanisms that connect gene regulation and 3D epithelial morphogenesis. Here we review the current understanding of this system, emphasizing how the recent identification of cis-regulatory regions of genes within the eggshell patterning network enables mechanistic analysis of its spatiotemporal dynamics and evolutionary diversification. It appears that cis-regulatory changes can account for only some aspects of the morphological diversity of Drosophila eggshells, such as the prominent differences in the number of the respiratory dorsal appendages. Other changes, such as the appearance of the respiratory eggshell ridges, are caused by changes in the spatial distribution of inductive signals. Both types of mechanisms are at play in this rapidly evolving system, which provides an excellent model of developmental patterning and morphogenesis.
3

Ahringer, J. "Maternal control of a zygotic patterning gene in Caenorhabditis elegans." Development 124, no. 19 (October 1, 1997): 3865–69. http://dx.doi.org/10.1242/dev.124.19.3865.

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The transition from maternal to zygotic gene control is a key process in embryogenesis. Although many maternal effect genes have been studied in the C. elegans embryo, how their activities lead to the positional expression of zygotic patterning genes has not yet been established. Evidence is presented showing that expression of the zygotic patterning gene vab-7 does not depend on cell position or cell contacts, but rather on the production of a C blastomere. Furthermore, pal-1, a caudal homologue with maternal product necessary for the proper development of the C blastomere, is both necessary and sufficient for vab-7 expression. This provides a link between maternal gene activity and zygotic patterning gene expression in C. elegans. The results suggest that zygotic patterning genes might be generally controlled at the level of blastomere fate and not by position.
4

Deyholos, M. K., G. Cordner, D. Beebe, and L. E. Sieburth. "The SCARFACE gene is required for cotyledon and leaf vein patterning." Development 127, no. 15 (August 1, 2000): 3205–13. http://dx.doi.org/10.1242/dev.127.15.3205.

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Mechanisms controlling vein patterning are poorly understood. We describe a recessive Arabidopsis mutant, scarface (sfc), which maps to chromosome 5. sfc mutants have vein pattern defects in cotyledons, leaves, sepals and petals. In contrast to the wild type, in which these organs all have linear veins that are continuous with at least one other vein, in sfc mutants these organs' secondary and tertiary veins are largely replaced by small segments of discontinuous veins, which we call vascular islands. Patterning defects are manifest in cotyledon provascular tissue, suggesting that the patterning defect occurs early in organogenesis. sfc mutants have exaggerated responses to exogenous auxin. Analysis of monopteros (mp(T370)) sfc-1 double mutants suggested that SFC has partially overlapping functions with MP in patterning of both primary and secondary veins.
5

Corbett, Daniel C., Wesley B. Fabyan, Bagrat Grigoryan, Colleen E. O’Connor, Fredrik Johansson, Ivan Batalov, Mary C. Regier, Cole A. DeForest, Jordan S. Miller, and Kelly R. Stevens. "Thermofluidic heat exchangers for actuation of transcription in artificial tissues." Science Advances 6, no. 40 (September 2020): eabb9062. http://dx.doi.org/10.1126/sciadv.abb9062.

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Spatial patterns of gene expression in living organisms orchestrate cell decisions in development, homeostasis, and disease. However, most methods for reconstructing gene patterning in 3D cell culture and artificial tissues are restricted by patterning depth and scale. We introduce a depth- and scale-flexible method to direct volumetric gene expression patterning in 3D artificial tissues, which we call “heat exchangers for actuation of transcription” (HEAT). This approach leverages fluid-based heat transfer from printed networks in the tissues to activate heat-inducible transgenes expressed by embedded cells. We show that gene expression patterning can be tuned both spatially and dynamically by varying channel network architecture, fluid temperature, fluid flow direction, and stimulation timing in a user-defined manner and maintained in vivo. We apply this approach to activate the 3D positional expression of Wnt ligands and Wnt/β-catenin pathway regulators, which are major regulators of development, homeostasis, regeneration, and cancer throughout the animal kingdom.
6

Cooper, Rory L., Alexandre P. Thiery, Alexander G. Fletcher, Daniel J. Delbarre, Liam J. Rasch, and Gareth J. Fraser. "An ancient Turing-like patterning mechanism regulates skin denticle development in sharks." Science Advances 4, no. 11 (November 2018): eaau5484. http://dx.doi.org/10.1126/sciadv.aau5484.

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Vertebrates have a vast array of epithelial appendages, including scales, feathers, and hair. The developmental patterning of these diverse structures can be theoretically explained by Alan Turing’s reaction-diffusion system. However, the role of this system in epithelial appendage patterning of early diverging lineages (compared to tetrapods), such as the cartilaginous fishes, is poorly understood. We investigate patterning of the unique tooth-like skin denticles of sharks, which closely relates to their hydrodynamic and protective functions. We demonstrate through simulation models that a Turing-like mechanism can explain shark denticle patterning and verify this system using gene expression analysis and gene pathway inhibition experiments. This mechanism bears remarkable similarity to avian feather patterning, suggesting deep homology of the system. We propose that a diverse range of vertebrate appendages, from shark denticles to avian feathers and mammalian hair, use this ancient and conserved system, with slight genetic modulation accounting for broad variations in patterning.
7

Solari, F., A. Bateman, and J. Ahringer. "The Caenorhabditis elegans genes egl-27 and egr-1 are similar to MTA1, a member of a chromatin regulatory complex, and are redundantly required for embryonic patterning." Development 126, no. 11 (June 1, 1999): 2483–94. http://dx.doi.org/10.1242/dev.126.11.2483.

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We show here that two functionally redundant Caenorhabditis elegans genes, egl-27 and egr-1, have a fundamental role in embryonic patterning. When both are inactivated, cells in essentially all regions of the embryo fail to be properly organised. Tissue determination and differentiation are unaffected and many zygotic patterning genes are expressed normally, including HOX genes. However, hlh-8, a target of the HOX gene mab-5, is not expressed. egl-27 and egr-1 are members of a gene family that includes MTA1, a human gene with elevated expression in metastatic carcinomas. MTA1 is a component of a protein complex with histone deacetylase and nucleosome remodelling activities. We propose that EGL-27 and EGR-1 function as part of a chromatin regulatory complex required for the function of regional patterning genes.
8

Patel, Nipam H. "The evolution of arthropod segmentation: insights from comparisons of gene expression patterns." Development 1994, Supplement (January 1, 1994): 201–7. http://dx.doi.org/10.1242/dev.1994.supplement.201.

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The comparison of gene expression patterns in a number of insect and crustacean species has led to some insight into the evolution of arthropod patterning mechanisms. These studies have revealed the fundamental nature of the parasegment in a number of organisms, shown that segments can be generated sequentially at the molecular level, and suggested that pair-rule pre-patterning might not be shared by all insects.
9

Özdemir and Gambetta. "The Role of Insulation in Patterning Gene Expression." Genes 10, no. 10 (September 28, 2019): 767. http://dx.doi.org/10.3390/genes10100767.

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Development is orchestrated by regulatory elements that turn genes ON or OFF in precise spatial and temporal patterns. Many safety mechanisms prevent inappropriate action of a regulatory element on the wrong gene promoter. In flies and mammals, dedicated DNA elements (insulators) recruit protein factors (insulator binding proteins, or IBPs) to shield promoters from regulatory elements. In mammals, a single IBP called CCCTC-binding factor (CTCF) is known, whereas genetic and biochemical analyses in Drosophila have identified a larger repertoire of IBPs. How insulators function at the molecular level is not fully understood, but it is currently thought that they fold chromosomes into conformations that affect regulatory element-promoter communication. Here, we review the discovery of insulators and describe their properties. We discuss recent genetic studies in flies and mice to address the question: Is gene insulation important for animal development? Comparing and contrasting observations in these two species reveal that they have different requirements for insulation, but that insulation is a conserved and critical gene regulation strategy.
10

Vakulenko, Sergei, and Ovidiu Radulescu. "Flexible and Robust Patterning by Centralized Gene Networks." Fundamenta Informaticae 118, no. 4 (2012): 345–69. http://dx.doi.org/10.3233/fi-2012-719.

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Статті в журналах Дисертації

Дисертації з теми "Gene patterning":

1

Sauers, Daniel J. "Light directed gene patterning using photocaged doxycycline /." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 196 p, 2010. http://proquest.umi.com/pqdweb?did=1993328811&sid=6&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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2

Mellick, Albert S. Jr, and n/a. "Tissue Specific Gene Expression Patterning and Carcinogenesis." Griffith University. School of Health Science, 2004. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20041102.114313.

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Despite significant advances in diagnosis and treatment, breast cancer remains the leading cause of cancer-related deaths in Australian women. Colorectal cancer is the second most common cancer in both males and females; after prostate and breast cancer, respectively, and excluding non-melanocytic skin cancer. Both breast cancer and colorectal cancer follow a common progressive course of illness; presenting (at least initially) with benign symptoms that can be treated by ablation (or removal) of the affected area. Cancer progression is associated with breakdown of tissue barriers (such as basement membranes), leading to the spread of cancer cells (via the vasculature or lymphatic system), and the establishment of secondary metastatic disease at green-field sites. Secondary tumours presenting in the lungs, ovaries, liver, bone, or brain are associated with chronic-debilitating symptoms that are difficult to treat, and will result in death. In the case of breast and colon cancer, effective early therapeutic intervention does have a significant impact upon patient survival. Tumour progression in breast and colon carcinomas is characterised by invasion of the surrounding stroma, and the acquisition of stromal characteristics, by previously epithelial cells. This progression is associated with the expression of extracellular proteases (ECPs) and increased motility. The process of mesenchymal transformation that tumour cells undergo is also referred to as the epithelial to mesenchymal transition (EMT). In general terms the aim of the study, presented in this thesis, was to investigate gene expression in cancer biology; and to characterise changes in breast cancer and colon cancer, with a focus on those genes, and gene products that may play a role in metastasis, including a family of ECPs, the matrix metalloproteinases (MMPs). In our laboratory, we have applied methods in microdissection, differential display polymerase chain reaction amplification (DD-PCR), and array hybridisation analysis to identify gene expression patterns in late stage archival formalin fixed paraffin embedded (FFPE) breast tumour biopsies that may be indicative of the EMT; or the response to the surrounding stroma/interstitium to the presence of the tumour.' The quality of nucleic acid obtainable from FFPE material presents a considerable challenge for gene expression studies. In order to identify tissue specific gene expression patterns, DD-PCR products, amplified from message obtained following segregation of tumour tissue from surrounding stroma, was hybridised to arrayed cDNA libraries created from stromal tumours, or sarcomas. In this way, 21 known genes, or expressed sequence tags (ESTs), were identified. These included the cytoskeletal element and EMT marker, vimentin, the mammary developmental factor and, signal transducer and activator of transcription (STAT)-3, and the cargo selection protein (TIP47). Seventeen genes showed differential expression in either the tumour, or stromal fractions. When applied to transformed breast cancer cell lines (MDA-MB-435 & T47D) DD-array analysis revealed a further 17 genes that were differentially regulated in invasive cells, compared with those displaying a less invasive phenotype. Six of the ESTs identified by DD-PCR array analysis, had no known (or predicted) function. For example, bcaf-2 was identified as the 3'-end of a putative open reading frame (ORF) localised to chromosome 6, while bcaf-10 showed homology with a known ORF. In order to analyse the expression of these bcafs further, a stromal cell culture model, representative of the original osteosarcoma cDNA libraries from which they were obtained, was used. In this model, CD14' (or adherent) peripheral blood mononuclear cells (PBMCs) treated with macrophage colony stimulating factor (M-CSF), can be allowed to differentiate into macrophage-like (ML) cells; while cells treated with M-CSF, and the receptor activator of NF-KB ligand (RANKL) will differentiate into multinucleate osteoclast-like (OCL) multinucleate giant cells. Uniquely, the stromal EST, bcaf-2 was expressed only by RANKL-treated (or OCL) cells. bcaf-2 and other ESTs, identified by DD-PCR analysis (and recently published) are the subject of on going research in our laboratory. The role of RANKL in mammary gland development and bone metastasis suggested that the identification of a RANKL-regulated stromal factor in breast tissue (bcaf-2) was not an artefact. RANKL is a membrane-bound, member of the tumour necrosis factor (TNF)-a cytokine super family. In order to test the hypothesis that RANKL might act as an inflammatory cytokine to regulate clinically significant stromal gene expression in the breast, we employed quantitative real time PCR analysis to examine the relative levels of selected members of a group of metal dependent ECPs, the matrix metalloproteinases (MMPs). RNA was extracted from ML cells and OCL cells, as well as RANK positive breast cancer cell lines (T47D, MDA-MB-435 & MCF-7). When the relative levels of protease mRNA were compared we demonstrated a significant (>20- fold) specific increase in collagenase (collagenase 2lMMP-8 and collagenase 3lMMP-13), and the tissue inhibitor of MMP (TIMP)-2 expression in M-CSF and RANKL treated PBMCs cells. When the assay was applied to RANKL treated breast cancer cell lines (MCF-7, T47D & MDAMB- 231), minor (40-fold) but potentially significant alterations in stromal protease gene expression were observed. The changes observed did not however, support the hypothesis that RANKL might act as an inflammatory cytokine to induce significant alterations in ECP expression in breast cancer cells. To investigate the role of RANKL as a driver of EMT in aberrant breast epithelium, total message (mRNNcDNA) from T47D, MCF-7, MDA-MB-231 cells, and message from the same cell lines treated with RANKL were compared by comparative fluorescent cDNA microarray analysis. Of the 1,700 targets available on the arrays, this study identified 160 that were differentially expressed in RANKL treated cells. The results suggest that RANKL may promote rather than suppress a mammary epithelial phenotype in breast cancer. In fact a putative mesenchymal to epithelial transition (MET) was observed following microscopic analysis, and this finding is the subject of on going research in our laboratory. Sporadic structural alterations in certain mitogenic factors represent important early events in cancer progression, while inherited mutations govern familial susceptibility to disease. In colon cancer, a close link exists between Winglessllnt (WNT) signalling, disease pathology, and the expression of MMPs. To examine the relationship between protease expression and structural genetic alterations in this EMT-linked signalling pathway, and others, we applied combined QPCR analysis of MMP expression and PCR-Single Strand Conformation Analysis (SSCA) to 26 colonic tumours, and patient-matched normal colonic mucosa. In this study, significant correlations between the expression of ECPs, and a key mediator of WNT signalling (p-catenin) were identified. While tumours possessing specific functional mutations in K-Ras, were found to group with phenotypic clustering based on protease gene expression. This result may be due to an interruption of normal interactions between RasIRaf signalling and transforming growth factor (TGF) P signalling, via Sma- and Mad- related protein (SMAD) signalling. These results demonstrate that the already identified link between mutations in kinase signalling, and aspects of gross colon tumour morphology (such as dysplasia) may be due to aberrant MMP expression patterning. The final aim of this research was to utilise methods developed in microdissection and specific Q-PCR analysis, to identify whether tumour-stroma differences in MMP gene expression might be used as markers of disease pathology. Total RNA from tumour, and biopsy-matched adjacent stromal tissue were segregated from 35 FFPE archival breast tumour biopsies. Comparison with stroma identified specific associations between TIMP-2 expression in the stroma and lymph node involvement, as well as stromelysin-3 (MMP-I I ) and TIMP-I expression and calcification of the tumour. Furthermore, a significant correlation was identified in the pattern of gelatinase (gelatinase AIMMP-2 & gelatinaseB1MMP-9) expression; while no significant correlation was identified in tumour-stroma MMP gene expression differences, and tumour grade, or hormone receptor status. These results suggest that coordinated changes within the tumour, and proximal stromal tissues (rather than tissue specific changes per se), regulate pathologically significant changes in breast carcinogenesis. In conclusion, this thesis describes the use of novel techniques in specific and global gene expression analysis that permitted examination of stromal gene expression changes in epithelial tumour progression. Microdissection facilitated localisation of expression to particular tissues, while cell culture models provided material with which to optimise and demonstrate the efficacy of techniques used (where tumour material itself was not abundant). Furthermore, we have identified significant and specific correlations between general stromal protease gene expression changes, a putative mammary epithelial differentiation factor (RANKL), alterations in growth factor signalling, and epithelial tumour pathology in the breast and colon. The combination of techniques developed in this study may assist in improvement of categorisation of tumours in clinical pathology. Specifically, the development of novel grading systems that link underlying molecular genetic changes with changes in tumour pathology. These processes may assist to improve diagnosis and provide more effective patient/tumour-specific drug therapies.
3

Mellick, Albert S. Jr. "Tissue Specific Gene Expression Patterning and Carcinogenesis." Thesis, Griffith University, 2004. http://hdl.handle.net/10072/365189.

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Despite significant advances in diagnosis and treatment, breast cancer remains the leading cause of cancer-related deaths in Australian women. Colorectal cancer is the second most common cancer in both males and females; after prostate and breast cancer, respectively, and excluding non-melanocytic skin cancer. Both breast cancer and colorectal cancer follow a common progressive course of illness; presenting (at least initially) with benign symptoms that can be treated by ablation (or removal) of the affected area. Cancer progression is associated with breakdown of tissue barriers (such as basement membranes), leading to the spread of cancer cells (via the vasculature or lymphatic system), and the establishment of secondary metastatic disease at green-field sites. Secondary tumours presenting in the lungs, ovaries, liver, bone, or brain are associated with chronic-debilitating symptoms that are difficult to treat, and will result in death. In the case of breast and colon cancer, effective early therapeutic intervention does have a significant impact upon patient survival. Tumour progression in breast and colon carcinomas is characterised by invasion of the surrounding stroma, and the acquisition of stromal characteristics, by previously epithelial cells. This progression is associated with the expression of extracellular proteases (ECPs) and increased motility. The process of mesenchymal transformation that tumour cells undergo is also referred to as the epithelial to mesenchymal transition (EMT). In general terms the aim of the study, presented in this thesis, was to investigate gene expression in cancer biology; and to characterise changes in breast cancer and colon cancer, with a focus on those genes, and gene products that may play a role in metastasis, including a family of ECPs, the matrix metalloproteinases (MMPs). In our laboratory, we have applied methods in microdissection, differential display polymerase chain reaction amplification (DD-PCR), and array hybridisation analysis to identify gene expression patterns in late stage archival formalin fixed paraffin embedded (FFPE) breast tumour biopsies that may be indicative of the EMT; or the response to the surrounding stroma/interstitium to the presence of the tumour.' The quality of nucleic acid obtainable from FFPE material presents a considerable challenge for gene expression studies. In order to identify tissue specific gene expression patterns, DD-PCR products, amplified from message obtained following segregation of tumour tissue from surrounding stroma, was hybridised to arrayed cDNA libraries created from stromal tumours, or sarcomas. In this way, 21 known genes, or expressed sequence tags (ESTs), were identified. These included the cytoskeletal element and EMT marker, vimentin, the mammary developmental factor and, signal transducer and activator of transcription (STAT)-3, and the cargo selection protein (TIP47). Seventeen genes showed differential expression in either the tumour, or stromal fractions. When applied to transformed breast cancer cell lines (MDA-MB-435 & T47D) DD-array analysis revealed a further 17 genes that were differentially regulated in invasive cells, compared with those displaying a less invasive phenotype. Six of the ESTs identified by DD-PCR array analysis, had no known (or predicted) function. For example, bcaf-2 was identified as the 3'-end of a putative open reading frame (ORF) localised to chromosome 6, while bcaf-10 showed homology with a known ORF. In order to analyse the expression of these bcafs further, a stromal cell culture model, representative of the original osteosarcoma cDNA libraries from which they were obtained, was used. In this model, CD14' (or adherent) peripheral blood mononuclear cells (PBMCs) treated with macrophage colony stimulating factor (M-CSF), can be allowed to differentiate into macrophage-like (ML) cells; while cells treated with M-CSF, and the receptor activator of NF-KB ligand (RANKL) will differentiate into multinucleate osteoclast-like (OCL) multinucleate giant cells. Uniquely, the stromal EST, bcaf-2 was expressed only by RANKL-treated (or OCL) cells. bcaf-2 and other ESTs, identified by DD-PCR analysis (and recently published) are the subject of on going research in our laboratory. The role of RANKL in mammary gland development and bone metastasis suggested that the identification of a RANKL-regulated stromal factor in breast tissue (bcaf-2) was not an artefact. RANKL is a membrane-bound, member of the tumour necrosis factor (TNF)-a cytokine super family. In order to test the hypothesis that RANKL might act as an inflammatory cytokine to regulate clinically significant stromal gene expression in the breast, we employed quantitative real time PCR analysis to examine the relative levels of selected members of a group of metal dependent ECPs, the matrix metalloproteinases (MMPs). RNA was extracted from ML cells and OCL cells, as well as RANK positive breast cancer cell lines (T47D, MDA-MB-435 & MCF-7). When the relative levels of protease mRNA were compared we demonstrated a significant (>20- fold) specific increase in collagenase (collagenase 2lMMP-8 and collagenase 3lMMP-13), and the tissue inhibitor of MMP (TIMP)-2 expression in M-CSF and RANKL treated PBMCs cells. When the assay was applied to RANKL treated breast cancer cell lines (MCF-7, T47D & MDAMB- 231), minor (40-fold) but potentially significant alterations in stromal protease gene expression were observed. The changes observed did not however, support the hypothesis that RANKL might act as an inflammatory cytokine to induce significant alterations in ECP expression in breast cancer cells. To investigate the role of RANKL as a driver of EMT in aberrant breast epithelium, total message (mRNNcDNA) from T47D, MCF-7, MDA-MB-231 cells, and message from the same cell lines treated with RANKL were compared by comparative fluorescent cDNA microarray analysis. Of the 1,700 targets available on the arrays, this study identified 160 that were differentially expressed in RANKL treated cells. The results suggest that RANKL may promote rather than suppress a mammary epithelial phenotype in breast cancer. In fact a putative mesenchymal to epithelial transition (MET) was observed following microscopic analysis, and this finding is the subject of on going research in our laboratory. Sporadic structural alterations in certain mitogenic factors represent important early events in cancer progression, while inherited mutations govern familial susceptibility to disease. In colon cancer, a close link exists between Winglessllnt (WNT) signalling, disease pathology, and the expression of MMPs. To examine the relationship between protease expression and structural genetic alterations in this EMT-linked signalling pathway, and others, we applied combined QPCR analysis of MMP expression and PCR-Single Strand Conformation Analysis (SSCA) to 26 colonic tumours, and patient-matched normal colonic mucosa. In this study, significant correlations between the expression of ECPs, and a key mediator of WNT signalling (p-catenin) were identified. While tumours possessing specific functional mutations in K-Ras, were found to group with phenotypic clustering based on protease gene expression. This result may be due to an interruption of normal interactions between RasIRaf signalling and transforming growth factor (TGF) P signalling, via Sma- and Mad- related protein (SMAD) signalling. These results demonstrate that the already identified link between mutations in kinase signalling, and aspects of gross colon tumour morphology (such as dysplasia) may be due to aberrant MMP expression patterning. The final aim of this research was to utilise methods developed in microdissection and specific Q-PCR analysis, to identify whether tumour-stroma differences in MMP gene expression might be used as markers of disease pathology. Total RNA from tumour, and biopsy-matched adjacent stromal tissue were segregated from 35 FFPE archival breast tumour biopsies. Comparison with stroma identified specific associations between TIMP-2 expression in the stroma and lymph node involvement, as well as stromelysin-3 (MMP-I I ) and TIMP-I expression and calcification of the tumour. Furthermore, a significant correlation was identified in the pattern of gelatinase (gelatinase AIMMP-2 & gelatinaseB1MMP-9) expression; while no significant correlation was identified in tumour-stroma MMP gene expression differences, and tumour grade, or hormone receptor status. These results suggest that coordinated changes within the tumour, and proximal stromal tissues (rather than tissue specific changes per se), regulate pathologically significant changes in breast carcinogenesis. In conclusion, this thesis describes the use of novel techniques in specific and global gene expression analysis that permitted examination of stromal gene expression changes in epithelial tumour progression. Microdissection facilitated localisation of expression to particular tissues, while cell culture models provided material with which to optimise and demonstrate the efficacy of techniques used (where tumour material itself was not abundant). Furthermore, we have identified significant and specific correlations between general stromal protease gene expression changes, a putative mammary epithelial differentiation factor (RANKL), alterations in growth factor signalling, and epithelial tumour pathology in the breast and colon. The combination of techniques developed in this study may assist in improvement of categorisation of tumours in clinical pathology. Specifically, the development of novel grading systems that link underlying molecular genetic changes with changes in tumour pathology. These processes may assist to improve diagnosis and provide more effective patient/tumour-specific drug therapies.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Health Sciences
Faculty of Health Sciences
Full Text
4

Blader, Patrick. "Analysis of gene expression during early development of the zebrafish, Brachydanio rerio." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282415.

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5

Boehm, Christian Reiner. "Gene expression control for synthetic patterning of bacterial populations and plants." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/267842.

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The development of shape in multicellular organisms has intrigued human minds for millenia. Empowered by modern genetic techniques, molecular biologists are now striving to not only dissect developmental processes, but to exploit their modularity for the design of custom living systems used in bioproduction, remediation, and regenerative medicine. Currently, our capacity to harness this potential is fundamentally limited by a lack of spatiotemporal control over gene expression in multicellular systems. While several synthetic genetic circuits for control of multicellular patterning have been reported, hierarchical induction of gene expression domains has received little attention from synthetic biologists, despite its fundamental role in biological self-organization. In this thesis, I introduce the first synthetic genetic system implementing population-based AND logic for programmed hierarchical patterning of bacterial populations of Escherichia coli, and address fundamental prerequisites for implementation of an analogous genetic circuit into the emergent multicellular plant model Marchantia polymorpha. In both model systems, I explore the use of bacteriophage T7 RNA polymerase as a gene expression engine to control synthetic patterning across populations of cells. In E. coli, I developed a ratiometric assay of bacteriophage T7 RNA polymerase activity, which I used to systematically characterize different intact and split enzyme variants. I utilized the best-performing variant to build a three-color patterning system responsive to two different homoserine lactones. I validated the AND gate-like behavior of this system both in cell suspension and in surface culture. Then, I used the synthetic circuit in a membrane-based spatial assay to demonstrate programmed hierarchical patterning of gene expression across bacterial populations. To prepare the adaption of bacteriophage T7 RNA polymerase-driven synthetic patterning from the prokaryote E. coli to the eukaryote M. polymorpha, I developed a toolbox of genetic elements for spatial gene expression control in the liverwort: I analyzed codon usage across the transcriptome of M. polymorpha, and used insights gained to design codon-optimized fluorescent reporters successfully expressed from its nuclear and chloroplast genomes. For targeting of bacteriophage T7 RNA polymerase to these cellular compartments, I functionally validated nuclear localization signals and chloroplast transit peptides. For spatiotemporal control of bacteriophage T7 RNA polymerase in M. polymorpha, I characterized spatially restricted and inducible promoters. For facilitated posttranscriptional processing of target transcripts, I functionally validated viral enhancer sequences in M. polymorpha. Taking advantage of this genetic toolbox, I introduced inducible nuclear-targeted bacteriophage T7 RNA polymerase into M. polymorpha. I showed implementation of the bacteriophage T7 RNA polymerase/PT7 expression system accompanied by hypermethylation of its target nuclear transgene. My observations suggest operation of efficient epigenetic gene silencing in M. polymorpha, and guide future efforts in chassis engineering of this multicellular plant model. Furthermore, my results encourage utilization of spatiotemporally controlled bacteriophage T7 RNA polymerase as a targeted silencing system for functional genomic studies and morphogenetic engineering in the liverwort. Taken together, the work presented enhances our capacity for spatiotemporal gene expression control in bacterial populations and plants, facilitating future efforts in synthetic morphogenesis for applications in synthetic biology and metabolic engineering.
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Jackman, William R. "Segmentation and molecular patterning of the amphioxus hindbrain, pharynx, and somites /." view abstract or download file of text, 2000. http://wwwlib.umi.com/cr/uoregon/fullcit?p9998038.

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Thesis (Ph. D.)--University of Oregon, 2000.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 96-105). Also available for download via the World Wide Web; free to University of Oregon users.
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Buxton, Paul Graeme. "Embryonic roles for the slug regulatory gene in hindbrain regulation and limb patterning." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266133.

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8

McKnight, Kristen Dawn. "Gene expression profiling reveals novel attributes of the mouse definitive endoderm." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/3431.

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Gastrulation is one of the most critical events of embryogenesis, generating the three primary germ layers (definitive endoderm, mesoderm, and ectoderm) and establishing the embryonic body plan. The definitive endoderm, which generates the lungs, liver, pancreas, and digestive tract, has become a tissue of particular interest in recent years. Understanding definitive endoderm formation and patterning will greatly aid progress in the in vitro differentiation of embryonic stem cells to definitive endoderm for use in treatment of diseases such as diabetes and hepatitis as an alternative for whole organ replacement. Gene targeting studies have demonstrated a critical role for the Nodal signaling pathway and the forkhead transcription factors Foxh1 and Foxa2 in specification of a group of cells referred to as the anterior primitive streak (APS). However, the transcriptional targets of Foxh1 and/or Foxa2 other than Nodal that regulate specification of this group of cells are currently unknown. Fate mapping and lineage tracing experiments have shown the APS to be the source of the definitive endoderm. However, many questions regarding specification and patterning of the definitive endoderm remain. The study of this tissue has been hampered by the lack of genetic markers specific for the definitive endoderm as many of the current markers, including Cerl, Foxa2, and Sox17, are also expressed in the visceral endoderm, an extraembryonic tissue. To further investigate the role of Foxh1 in specification of the anterior primitive streak and to address the lack of genetic markers for the definitive endoderm we performed expression profiling on post-implantation mouse embryos using Affymetrix™ GeneChips®. From this analysis we identified and characterized a novel marker of the mouse definitive endoderm. Examination of this, and other, novel endoderm markers in Foxh1 and Foxa2 deficient mouse embryos revealed that contrary to current models of definitive endoderm formation, we find some definitive endoderm is formed in these mutants. Specifically, specification of the midgut and hindgut definitive endoderm is largely unaffected, while foregut formation is severely affected. These results suggest that the formation of the midgut and hindgut definitive endoderm populations is independent of the anterior primitive streak and separate from the foregut definitive endoderm. This represents a major insight into the mechanisms regulating endoderm formation and patterning.
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Yamamoto, Mako. "The transformation suppressor gene Reck is required for postaxial patterning in mouse forelimbs." Kyoto University, 2012. http://hdl.handle.net/2433/158062.

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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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Книги з теми "Gene patterning":

1

Thomas, Lufkin, ed. Murine homeobox gene control of embryonic patterning and organogenesis. Amsterdam: Elsevier, 2003.

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2

Murine Homeobox Gene Control of Embryonic Patterning and Organogenesis. Elsevier, 2003. http://dx.doi.org/10.1016/s1569-1799(00)x0002-0.

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3

Lufkin, T. Murine Homeobox Gene Control of Embryonic Patterning and Organogenesis. Elsevier Science & Technology Books, 2003.

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4

Lufkin, T. Murine Homeobox Gene Control of Embryonic Patterning and Organogenesis (Advances in Developmental Biology and Biochemistry). Elsevier Science, 2003.

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5

Lebel, Melanie. The role of Shh, Gli and Irx genes during mouse neural patterning. 2006.

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6

Berliner, Todd. Classicism and Deviation in His Girl Friday and Double Indemnity. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780190658748.003.0002.

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Chapter 2 illustrates an aesthetically productive balance between easy understanding and cognitive challenge in classical Hollywood cinema with extended analyses of His Girl Friday and Double Indemnity. These films combine classical narrative, stylistic, ideological, and genre properties with artistic devices that complicate formal patterning and thwart audience expectations.
7

Kamei, Caramai Nanae. Patterning the vertebate mesoderm: Functional analysis of bone morphogenetic protein-responsive genes in vasculogenesis and kidney development. 2010.

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8

Cahill, Thomas J., and Paul R. Riley. Epicardial and coronary vascular development. Edited by Miguel Torres. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0009.

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The coronary circulation is essential for human life. In embryonic development, abnormal formation of the coronary vasculature can cause death in utero or after birth. In adulthood, atherosclerosis of the coronary arteries is the commonest cause of death worldwide. The last decade has witnessed significant strides forward in our understanding of coronary development. Multiple sources of coronary endothelial cells have been identified using genetic tools for fate mapping. The epicardium, the outermost layer of the developing heart, has emerged as both a source of cell progenitors and key signalling mediators. Knowledge of the specific genes underlying formation, function, and heterogeneity of the epicardium is expanding. Significant challenges remain, however, in understanding the spatiotemporal signalling patterns required for organized migration, differentiation, and patterning of the vasculature. In addition, dissecting how coronary development is perturbed in patients with congenital coronary anomalies is a major ongoing focus of research.
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MacGrogan, Donal, José Maria Pérez-Pomares, Bill Chaudhry, José Luis de la Pompa, and Deborah J. Henderson. From cushions to leaflets: morphogenesis of cardiac atrioventricular valves. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0017.

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At the looping stage of heart development, tissue patterning of myocardium and endocardium at the atrioventricular (AV) junction defines a morphogenic field competent to form valves that initially appear as protrusions of proteoglycan-rich extracellular matrix (ECM) called endocardial cushions (ECs) which are cellularized by an endocardial-mesenchymal transition (EMT). Cellular proliferation results in fusion of the major AV mesenchymal cushions and AV septation, whereas smaller cushions receive a supply from epicardially derived cells. These various sources of mesenchyme precursors give rise to most of the valve structures, leaflets, annuli, and supporting tension apparatus. During valve leaflet maturation, the ECM matrix accumulates collagen and elastin and assembles into a thin flexible fibrous structure, which is remarkably tough. Valve development is regulated by the cross-talk between developmental signalling pathways. Pathogenic mutations in a subset of developmentally important genes have been linked to valve disease, suggesting that developmental defects may underlie valve disease in adulthood.

Частини книг з теми "Gene patterning":

1

Blundell, Patricia A., Jose-Luis de la Pompa, J. H. Carel Meijers, Andreas Trumpp, and Rolf Zeller. "The Limb Deformity Gene Encodes Evolutionarily Highly Conserved Proteins." In Developmental Patterning of the Vertebrate Limb, 25–30. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3310-8_4.

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2

Rowe, Annie, Nicholas S. C. Eager, Melanie Saville, Lewis Wolpert, and Paul M. Brickell. "Expression Pattern of an RXR Nuclear Receptor Gene in the Chick Embryo." In Developmental Patterning of the Vertebrate Limb, 101–4. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3310-8_15.

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3

Wudarski, Jakub, Kirill Ustyantsev, Filipa Reinoite, and Eugene Berezikov. "Random Integration Transgenesis in a Free-Living Regenerative Flatworm Macrostomum lignano." In Methods in Molecular Biology, 493–508. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2172-1_26.

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AbstractRegeneration-capable flatworms are highly informative research models to study the mechanisms of stem cell regulation, regeneration, and tissue patterning. Transgenesis is a powerful research tool for investigating gene function, but until recently, a transgenesis method was missing in flatworms, hampering their wider adoption in biomedical research. Here we describe a detailed protocol to create stable transgenic lines of the flatworm M. lignano using random integration of DNA constructs through microinjection into single-cell stage embryos.
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Tabin, Clifford J., Bruce Morgan, Hans-Georg Simon, Sara Lazar, Yaoqui Wang, Anuradha Iyer, Julia Yaglom, Changpin Shi, Ken Muneoka, and David Sassoon. "Functional Studies of Genes in the Limb." In Developmental Patterning of the Vertebrate Limb, 45–54. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3310-8_7.

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5

Akimenko, Marie-Andrée, Marc Ekker, and Monte Westerfield. "Characterization of Three Zebrafish Genes Related to Hox-7." In Developmental Patterning of the Vertebrate Limb, 61–63. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3310-8_10.

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6

Brown, Robin, and Jeremy P. Brockes. "The Role of Homeobox Genes in Amphibian Limb Development and Regeneration." In Developmental Patterning of the Vertebrate Limb, 31–35. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3310-8_5.

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7

Hill, Robert E., and Duncan R. Davidson. "Expression of the Msh-Like Homebox-Containing Genes during Mouse Limb Development." In Developmental Patterning of the Vertebrate Limb, 15–23. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3310-8_3.

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8

Kosher, Robert A., William B. Upholt, Caroline N. D. Coelho, Kimberly J. Blake, and Lauro Sumoy. "Homeobox-Containing Genes and GAP Junctional Communication in Pattern Formation during Chick Limb Development." In Developmental Patterning of the Vertebrate Limb, 37–43. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3310-8_6.

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9

O'Leary, Dennis D. M., Shen-Ju Chou, Tadashi Hamasaki, Setsuko Sahara, Akihide Takeuchi, Sandrine Thuret, and Axel Leingärtner. "Regulation of Laminar and Area Patterning of Mammalian Neocortex and Behavioural Implications." In Cortical Development: Genes and Genetic Abnormalities, 141–64. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470994030.ch11.

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10

Dollé, Pascal, Esther Ruberte, Juan-Carlos Izpisùa-Belmonte, Hildegard Falkenstein, Pierre Chambon, and Denis Duboule. "A Comparison of the Expression Domains of the Murine Hox-4, RARs and CRABP Genes Suggests Possible Functional Relationships During Patterning of the Vertebrate Limb." In Developmental Patterning of the Vertebrate Limb, 65–73. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3310-8_11.

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Тези доповідей конференцій з теми "Gene patterning":

1

Polstein, Lauren R., and Charles A. Gersbach. "Photoregulated Gene Expression in Human Cells With Light-Inducible Engineered Transcription Factors." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80573.

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Systems for controlling gene expression in mammalian cells have a wide range of applications in medicine, biotechnology and basic science. An ideal gene regulatory system would allow for precise and specific control over the magnitude and kinetics of gene expression in space and time, while also exerting minimal influence on other genes and cellular components. Several gene regulatory systems have been developed in which orthogonal transcription machinery from prokaryotes or insects has been imported into mammalian cells and used to control the expression of a specific gene. Despite the transformative impact of these systems in biomedical and biological research, several limitations of these technologies restrict the scope of possible applications. For example, gene expression in these systems is controlled by a freely diffusible small molecule, such as an antibiotic or steroid. Consequently, it is not possible to achieve spatial control over gene expression within cell culture, tissues, or whole organisms. This is in contrast to natural mechanisms of biological regulation in which spatial control is critical, such as developmental patterning and tissue morphogenesis. Second, dynamic gene regulation requires the removal of these small molecules, which may be slow, laborious, and/or impractical for a particular application. To overcome these limitations, we have engineered an optogenetic system in which the magnitude of gene expression in human cells can be finely tuned by photoregulated synthetic transcription factors.
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Mines, Robert C., Anders Dohlman, Sze-Xian Lim, Kuei-Ling Tung, Ergang Wang та Xiling Shen. "Spatial Patterning from an Integrated Wnt/β-catenin and Notch/Delta Gene Circuit". У 2018 40th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2018. http://dx.doi.org/10.1109/embc.2018.8513462.

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3

Hsia, Justin, William J. Holtz, Michel M. Maharbiz, and Murat Arcak. "New architecture for patterning gene expression using zinc finger proteins and small RNAs." In 2012 IEEE 51st Annual Conference on Decision and Control (CDC). IEEE, 2012. http://dx.doi.org/10.1109/cdc.2012.6426642.

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4

"THRESHOLD LOGIC GENE REGULATORY MODEL - Prediction of Dorsal-ventral Patterning and Hardware-based Simulation of Drosophila." In International Conference on Biomedical Electronics and Devices. SciTePress - Science and and Technology Publications, 2008. http://dx.doi.org/10.5220/0001054302120219.

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5

Trinh, Bon Q., Nicolas Barengo та Honami Naora. "Abstract B15: The homeobox patterning gene DLX4 confers resistance to transforming growth factor-β signaling in tumors". У Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-b15.

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6

Holloway, David M., and Alexander V. Spirov. "Gene expression noise in embryonic spatial patterning: Reliable formation of the head-to-tail axis in the fruit fly." In 2011 21st International Conference on Noise and Fluctuations (ICNF). IEEE, 2011. http://dx.doi.org/10.1109/icnf.2011.5994379.

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7

MARNELLOS, G., G. A. DEBLANDRE, E. MJOLSNESS, and C. KINTNER. "DELTA-NOTCH LATERAL INHIBITORY PATTERNING IN THE EMERGENCE OF CILIATED CELLS IN XENOPUS: EXPERIMENTAL OBSERVATIONS AND A GENE NETWORK MODEL." In Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 1999. http://dx.doi.org/10.1142/9789814447331_0031.

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8

Wang, Shuyang. "Analyzing Zelda and Other Transcription Factors That Regulating Ubiquitous and Patterning Genes of Drosophila Melanogaster." In The International Conference on Biomedical Engineering and Bioinformatics. SCITEPRESS - Science and Technology Publications, 2022. http://dx.doi.org/10.5220/0011297000003443.

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9

Gotoh, Hiroki. "The function of appendage patterning genes in extreme mandible development of a sexually dimorphic stag beetle." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.113157.

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10

Wynn, April. "Loss of flower and ovule patterning genes PAN and SEU increases sensitivity to drought, day-length and temperature stress in Arabidopsis thaliana." In ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.213479.

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Звіти організацій з теми "Gene patterning":

1

Ori, Naomi, and Mark Estelle. Role of GOBLET and Auxin in Controlling Organ Development and Patterning. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7697122.bard.

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The size and shape of plant leaves are extremely diverse within and among species, and are also sensitive to growth conditions. Compound leaves, such as those of tomato, maintain morphogenetic activity during early stages of their development, enabling them to elaborate lateral appendages such as leaflets. The aim of the research project was to understand the interaction between the plant hormone auxin, the putative auxin response inhibitor ENTIRE (E, SlIAA9) and the NAM/CUC transcription factor GOBLET (GOB) in compound-leaf development in tomato (Solanum lycopersicum). The specific aims of the project were: 1. Investigation of the role of GOB in compound-leaf development. 2. Characterization of E function in auxin signaling. 3. Characterization of the role of auxin in compound-leaf development. 4. Investigation of the genetic and molecular interaction between E and GOB. 5. Investigate the role of these factors in fruit development. There were no major changes in these objectives. GOB was shown to mark and promote the boundaries between the leaf and initiating leaflets. Its accurate distribution was found to be required for proper leaflet initiation and separation. E was found to interact with the TIR1 and AFB6 proteins in an auxin-dependant manner, indicating that these are functional auxin receptors that mediate E degradation in the presence of auxin. This was further supported by the stabilization of E by a mutation in domain II of the protein, which is thought to mediate its auxin-dependant degradation. Over expression of this stabilized form in tomato leaves and characterization of the e mutant phenotype and the E expression domain indicated that E acts between initiating leaflets to inhibit auxin response and lamina growth. Generation and analysis of tomato plants expressing the auxin response reporter DR5::VENUS, and analysis of the effect of auxin microapplication or overexpression of an auxin biosynthesis gene, indicated that auxin marks the sites of leaflet initiation and promotes lamina growth. Investigation of the molecular and genetic interaction between auxin, GOB and E revealed a complex network of mutual regulation that is utilized to precisely pattern the leaf margin in a manner that enables the combination of tight control and flexibility. E, auxin and GOB were shown to affect fruit development and fruit set, and in an extension of the project are currently utilized to identify new players that affect these processes. The research project yielded enhanced understanding of the mechanisms of compound leaf patterning and provided tools that will enable the manipulation of leaf shape and fruit set.
2

Bryant, Susan V., and David M. Gardiner. Homeobox Genes and Patterning of the Proximal-Distal Axis in Regenerating Limbs. Fort Belvoir, VA: Defense Technical Information Center, May 1996. http://dx.doi.org/10.21236/ada320044.

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