genesis最新文献

{"title":"Evidences of differential methylation in the genome during development in the cactophilic Drosophila species","authors":"Adriano S. Santos,&nbsp;Ester S. Ramos,&nbsp;Vera L. S. Valente-Gaiesky,&nbsp;Fábio de Melo Sene,&nbsp;Maura H. Manfrin","doi":"10.1002/dvg.23554","DOIUrl":"10.1002/dvg.23554","url":null,"abstract":"<div>\u0000 \u0000 <p>DNA methylation with 5-methylcytosine (5mC) has been reported in the genome of several eukaryotes, with marked differences between vertebrates and invertebrates. DNA methylation is poorly understood as its role in evolution in insects. <i>Drosophila gouveai</i> (cluster <i>Drosophila buzzatii</i>) presents larvae that develop obligatorily in necrotic tissues of cacti in nature, with the distribution of populations in South America, and plasticity of phenotypes in insect–plant interaction. We characterize organisms at developmental stages and analyze variations at multiple methylation-sensitive <i>loci</i> in pupae, and adult flies using methylation sensitive amplification polymorphism. We obtained 326 <i>loci</i> with CCGG targets in the genome of <i>D. gouveai</i>. Genomic regions with molecular lengths from 100 to 700 pb were most informative about methylation states. Multiple <i>loci</i> show differences in methylation-sensitive sites (MSL) concerning developmental stages, such as in pupae (MSL = 40), female reproductive tissue (MSL = 76), and male reproductive tissues (MSL = 58). Our results are the first evidence of genome-wide methylation in <i>D. gouveai</i> organisms.</p>\u0000 </div>","PeriodicalId":12718,"journal":{"name":"genesis","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41149647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"“Beyond transcription: How post-transcriptional mechanisms drive neural crest EMT”","authors":"Mariann Guzman-Espinoza,&nbsp;Minyoung Kim,&nbsp;Cindy Ow,&nbsp;Erica J. Hutchins","doi":"10.1002/dvg.23553","DOIUrl":"10.1002/dvg.23553","url":null,"abstract":"<p>The neural crest is a stem cell population that originates from the ectoderm during the initial steps of nervous system development. Neural crest cells delaminate from the neuroepithelium by undergoing a spatiotemporally regulated epithelial-mesenchymal transition (EMT) that proceeds in a coordinated wave head-to-tail to exit from the neural tube. While much is known about the transcriptional programs and membrane changes that promote EMT, there are additional levels of gene expression control that neural crest cells exert at the level of RNA to control EMT and migration. Yet, the role of post-transcriptional regulation, and how it drives and contributes to neural crest EMT, is not well understood. In this mini-review, we explore recent advances in our understanding of the role of post-transcriptional regulation during neural crest EMT.</p>","PeriodicalId":12718,"journal":{"name":"genesis","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvg.23553","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41171052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correlation between E-cadherin/β-catenin, Vimentin expression, clinicopathologic features and drug resistance prediction in naïve prostate cancer: A molecular and clinical study","authors":"Rahma Said,&nbsp;Javier Hernández-Losa,&nbsp;Amine Derouiche,&nbsp;Teresa Moline,&nbsp;Rosa Somoza Lopez de Haro,&nbsp;Skander Zouari,&nbsp;Ahlem Blel,&nbsp;Soumaya Rammeh,&nbsp;Slah Ouerhani","doi":"10.1002/dvg.23543","DOIUrl":"10.1002/dvg.23543","url":null,"abstract":"<div>\u0000 \u0000 <p>Although epithelial–mesenchymal markers play an important role in prostate cancer (PC), further research is needed to better understand their utility in diagnosis, cancer progression prevention, and treatment resistance prediction. Our study included 111 PC patients who underwent transurethral resection, as well as 16 healthy controls. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to examine the expression of E-cadherin, β-catenin, and Vimentin. We found that E-cadherin and β-catenin were underexpressed in primary PC tissues. E-cadherin expression was found to be inversely associated with prostate-specific antigen progression (PSA-P; serum marker of progression; <i>p</i> = 0.01; |r| = 0.262). Furthermore, the underexpression of two markers, E-cadherin and β-catenin, was found to be associated with advanced tumor stage and grade (<i>p</i> &lt; 0.05). On the other hand, Vimentin was overexpressed in PC patients with a fold change of 2.141, and it was associated with the diagnosis, prognosis, and prediction of treatment resistance to androgen deprivation therapy (<i>p</i> = 0.002), abiraterone-acid (<i>p</i> = 0.001), and taxanes (<i>p</i> = 0.029). Moreover, the current study highlighted that poor survival could be significantly found in patients who progressed after primary surgery, did not use drugs, and expressed these genes aberrantly. In Cox regression multivariate analysis (<i>p</i> &lt; 0.05), a positive correlation between the Vimentin marker and coronary heart disease in PC patients was identified (<i>p</i> = 0.034). In summary, the present study highlights the diagnostic (<i>p</i> &lt; 0.001), prognostic (<i>p</i> &lt; 0.001), and therapeutic potential of Vimentin in primary PC (<i>p</i> &lt; 0.05), as well as its implications for cardiovascular disease. Furthermore, we confirm the potential prognostic value of E-cadherin and β-catenin.</p>\u0000 </div>","PeriodicalId":12718,"journal":{"name":"genesis","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10122133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A temporally-restricted pattern of endothelial cell collagen 4 alpha 1 expression during embryonic development determined with a novel knockin Col4a1-P2A-eGFP mouse line","authors":"Nathaniel L. Lartey,&nbsp;Martijn van der Ent,&nbsp;Roxann Alonzo,&nbsp;Di Chen,&nbsp;Philip D. King","doi":"10.1002/dvg.23539","DOIUrl":"10.1002/dvg.23539","url":null,"abstract":"<p>Classical collagen type IV comprising of a heterotrimer of two collagen IV alpha 1 chains and one collagen IV alpha 2 chain is the principal type of collagen synthesized by endothelial cells (EC) and is a major constituent of vascular basement membranes. In mouse and man, mutations in genes that encode collagen IV alpha 1 and alpha 2 result in vascular dysfunction. In addition, mutations in genes that encode the Ephrin receptor B4 (EPHB4) and the p120 Ras GTPase-activating protein (RASA1) that cause increased activation of the Ras mitogen-activated protein kinase (MAPK) signaling pathway in EC result in vascular dysfunction as a consequence of impaired export of collagen IV. To understand the pathogenesis of collagen IV-related vascular diseases and phenotypes it is necessary to identify at which times collagen IV is actively synthesized by EC. For this purpose, we used CRISPR/Cas9 targeting in mice to include immediately after the terminal <i>Col4a1</i> codon a sequence that specifies a P2A peptide followed by enhanced green fluorescent protein (eGFP). Analysis of eGFP expression in <i>Col4a1-P2A-eGFP</i> mice revealed active embryonic EC synthesis of collagen IV alpha 1 through mid to late gestation followed by a sharp decline before birth. These results provide a contextual framework for understanding the basis for the varied vascular abnormalities resulting from perturbation of EC expression and export of functional collagen IV.</p>","PeriodicalId":12718,"journal":{"name":"genesis","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvg.23539","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10259891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cover Image, Volume 61, Issue 3–4","authors":"Vineet K. Maurya,&nbsp;Yan Ying,&nbsp;Denise G. Lanza,&nbsp;Jason D. Heaney,&nbsp;John P. Lydon","doi":"10.1002/dvg.23538","DOIUrl":"10.1002/dvg.23538","url":null,"abstract":"<p><b>Cover illustration:</b> The cover image is based on the Technical Note <i>A CRISPR/Cas9-engineered mouse carrying a conditional knockout allele for the early growth response-1 transcription factor</i> by Vineet K. Maurya et al., https://doi.org/10.1002/dvg.23515.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":12718,"journal":{"name":"genesis","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvg.23538","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47582984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resolving the mechanisms underlying epithelial-to-mesenchymal transition of the lateral plate mesoderm","authors":"Axel H. Newton,&nbsp;Craig A. Smith","doi":"10.1002/dvg.23531","DOIUrl":"10.1002/dvg.23531","url":null,"abstract":"<p>Formation of the vertebrate limb buds begins with a localized epithelial-to-mesenchymal transition (EMT) of the somatic lateral plate mesoderm (LPM). While the processes that drive proliferation and outgrowth of the limb mesenchyme are well established, the fundamental mechanisms that precede this process and initiate EMT are less understood. In this review, we outline putative drivers of EMT of the LPM, drawing from analyses across a range of vertebrates and developmental models. We detail the expression patterns of key EMT transcriptional regulators in the somatic LPM of the presumptive limb fields, and their potential role in producing a mesenchymal cell fate. These include a putative cooperative role between the EMT inducers PRRX1 and TWIST1, supported by evidence in zebrafish and chicken models but unconfirmed data from mice. As such, additional functional data are required to definitively determine the mechanisms that initiate and drive EMT of the somatic LPM, a critical transition preceding formation of the limb bud mesenchyme.</p>","PeriodicalId":12718,"journal":{"name":"genesis","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvg.23531","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9777330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Generation and characterization of a Dkk4-Cre knock-in mouse line","authors":"Houda Khatif,&nbsp;Hisham Bazzi","doi":"10.1002/dvg.23532","DOIUrl":"10.1002/dvg.23532","url":null,"abstract":"<p>Ectodermal appendages in mammals, such as teeth, mammary glands, sweat glands and hair follicles, are generated during embryogenesis through a series of mesenchymal–epithelial interactions. Canonical Wnt signaling and its inhibitors are implicated in the early steps of ectodermal appendage development and patterning. To study the activation dynamics of the Wnt target and inhibitor <i>Dickkopf4</i> (<i>Dkk4</i>) in ectodermal appendages, we used CRSIPR/Cas9 to generate a <i>Dkk4-Cre</i> knock-in mouse (<i>Mus musculus</i>) line, where the Cre recombinase cDNA replaces the expression of endogenous <i>Dkk4</i>. Using Cre reporters, the <i>Dkk4-Cre</i> activity was evident at the prospective sites of ectodermal appendages, overlapping with the <i>Dkk4</i> mRNA expression. Unexpectedly, a predominantly mesenchymal cell population in the embryo posterior also showed <i>Dkk4-Cre</i> activity. Lineage-tracing suggested that these cells are likely derived from a few <i>Dkk4-Cre</i>-expressing cells in the epiblast at early gastrulation. Finally, our analyses of <i>Dkk4-Cre</i>-expressing cells in developing hair follicle epithelial placodes revealed intra- and inter-placodal cellular heterogeneity, supporting emerging data on the positional and transcriptional cellular variability in placodes. Collectively, we propose the new <i>Dkk4-Cre</i> knock-in mouse line as a suitable model to study Wnt and DKK4 inhibitor dynamics in early mouse development and ectodermal appendage morphogenesis.</p>","PeriodicalId":12718,"journal":{"name":"genesis","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvg.23532","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10147566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel qPCR-based technique for identifying avian sex: An illustration within embryonic craniofacial bone","authors":"Claire J. Houchen,&nbsp;Maria Bergman-Gonzalez,&nbsp;Erin E. Bumann","doi":"10.1002/dvg.23530","DOIUrl":"10.1002/dvg.23530","url":null,"abstract":"<p>Sex is a biological variable important to consider in all biomedical experiments. However, doing so in avian embryos can be challenging as sex can be morphologically indistinguishable. Unlike humans, female birds are the heterogametic sex with Z and W sex chromosomes. The female-specific W chromosome has previously been identified in chick using a species-specific polymerase chain reaction (PCR) technique. We developed a novel reverse transcription quantitative PCR (RT-qPCR) technique that amplifies the W chromosome gene histidine triad nucleotide-binding protein W (<i>HINTW</i>) in chick<i>,</i> quail<i>,</i> and duck. Accuracy of the <i>HINTW</i> RT-qPCR primer set was confirmed in all three species using species-specific PCR, including a novel quail-specific <i>HINTW</i> PCR primer set. Bone development-related gene expression was then analyzed by sex in embryonic lower jaws of duck and quail, as adult duck beak size is known to be sexually dimorphic while quail beak size is not. Trends toward sex differences were found in duck gene expression but not in quail, as expected. With these novel RT-qPCR and PCR embryo sexing methods, sex of chick, quail, and duck embryos can now be assessed by either/both RNA and DNA, which facilitates analysis of sex as a biological variable in studies using these model organisms.</p>","PeriodicalId":12718,"journal":{"name":"genesis","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvg.23530","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10053454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epithelial–mesenchymal plasticity in kidney fibrosis","authors":"Sudarat Hadpech,&nbsp;Visith Thongboonkerd","doi":"10.1002/dvg.23529","DOIUrl":"10.1002/dvg.23529","url":null,"abstract":"<div>\u0000 \u0000 <p>Epithelial–mesenchymal transition (EMT) is an important biological process contributing to kidney fibrosis and chronic kidney disease. This process is characterized by decreased epithelial phenotypes/markers and increased mesenchymal phenotypes/markers. Tubular epithelial cells (TECs) are commonly susceptible to EMT by various stimuli, for example, transforming growth factor-β (TGF-β), cellular communication network factor 2, angiotensin-II, fibroblast growth factor-2, oncostatin M, matrix metalloproteinase-2, tissue plasminogen activator (t-PA), plasmin, interleukin-1β, and reactive oxygen species. Similarly, glomerular podocytes can undergo EMT via these stimuli and by high glucose condition in diabetic kidney disease. EMT of TECs and podocytes leads to tubulointerstitial fibrosis and glomerulosclerosis, respectively. Signaling pathways involved in EMT-mediated kidney fibrosis are diverse and complex. TGF-β1/Smad and Wnt/β-catenin pathways are the major venues triggering EMT in TECs and podocytes. These two pathways thus serve as the major therapeutic targets against EMT-mediated kidney fibrosis. To date, a number of EMT inhibitors have been identified and characterized. As expected, the majority of these EMT inhibitors affect TGF-β1/Smad and Wnt/β-catenin pathways. In addition to kidney fibrosis, these EMT-targeted antifibrotic inhibitors are expected to be effective for treatment against fibrosis in other organs/tissues.</p>\u0000 </div>","PeriodicalId":12718,"journal":{"name":"genesis","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9671422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expanding EMC foldopathies: Topogenesis deficits alter the neural crest","authors":"Jonathan Marquez,&nbsp;Faiza Aslam,&nbsp;Mustafa K. Khokha","doi":"10.1002/dvg.23520","DOIUrl":"10.1002/dvg.23520","url":null,"abstract":"<div>\u0000 \u0000 <p>The endoplasmic reticulum (ER) membrane protein complex (EMC) is essential for the insertion of a wide variety of transmembrane proteins into the plasma membrane across cell types. Each EMC is composed of Emc1-7, Emc10, and either Emc8 or Emc9. Recent human genetics studies have implicated variants in <i>EMC</i> genes as the basis for a group of human congenital diseases. The patient phenotypes are varied but appear to affect a subset of tissues more prominently than others. Namely, craniofacial development seems to be commonly affected. We previously developed an array of assays in <i>Xenopus tropicalis</i> to assess the effects of <i>emc1</i> depletion on the neural crest, craniofacial cartilage, and neuromuscular function. We sought to extend this approach to additional EMC components identified in patients with congenital malformations. Through this approach, we determine that EMC9 and EMC10 are important for neural crest development and the development of craniofacial structures. The phenotypes observed in patients and our <i>Xenopus</i> model phenotypes similar to <i>EMC1</i> loss of function likely due to a similar mechanism of dysfunction in transmembrane protein topogenesis.</p>\u0000 </div>","PeriodicalId":12718,"journal":{"name":"genesis","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvg.23520","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10663659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}