DevelopmentPub Date : 2024-10-15Epub Date: 2024-10-29DOI: 10.1242/dev.204442
Cassandra Extavour, Liam Dolan, Karen E Sears
{"title":"Promoting developmental diversity in a changing world.","authors":"Cassandra Extavour, Liam Dolan, Karen E Sears","doi":"10.1242/dev.204442","DOIUrl":"https://doi.org/10.1242/dev.204442","url":null,"abstract":"","PeriodicalId":11375,"journal":{"name":"Development","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142521317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DevelopmentPub Date : 2024-10-15Epub Date: 2024-09-14DOI: 10.1242/dev.202857
D Nathaniel Clarke, Akshay Kane, Margherita Perillo, Christopher J Lowe, S Zachary Swartz
{"title":"VitelloTag: a tool for high-throughput cargo delivery into oocytes.","authors":"D Nathaniel Clarke, Akshay Kane, Margherita Perillo, Christopher J Lowe, S Zachary Swartz","doi":"10.1242/dev.202857","DOIUrl":"10.1242/dev.202857","url":null,"abstract":"<p><p>Delivering molecular tools into oocytes is essential for developmental and reproductive biology. Microinjection, the conventional method, is equipment intensive, often technically challenging and has a low yield, and is impractical in species with delicate oocytes or restricted spawning seasons. To overcome these limitations, we developed VitelloTag, a cost-effective, high-throughput system using vitellogenin-derived fusion proteins to enable efficient cargo delivery via receptor-mediated endocytosis. We demonstrate its utility by delivering Cas9/sgRNA complexes in two distantly related species for gene knockout.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11423919/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142016668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DevelopmentPub Date : 2024-10-15Epub Date: 2024-10-17DOI: 10.1242/dev.203054
Áine McColgan, James DiFrisco
{"title":"Understanding developmental system drift.","authors":"Áine McColgan, James DiFrisco","doi":"10.1242/dev.203054","DOIUrl":"10.1242/dev.203054","url":null,"abstract":"<p><p>Developmental system drift (DSD) occurs when the genetic basis for homologous traits diverges over time despite conservation of the phenotype. In this Review, we examine the key ideas, evidence and open problems arising from studies of DSD. Recent work suggests that DSD may be pervasive, having been detected across a range of different organisms and developmental processes. Although developmental research remains heavily reliant on model organisms, extrapolation of findings to non-model organisms can be error-prone if the lineages have undergone DSD. We suggest how existing data and modelling approaches may be used to detect DSD and estimate its frequency. More direct study of DSD, we propose, can inform null hypotheses for how much genetic divergence to expect on the basis of phylogenetic distance, while also contributing to principles of gene regulatory evolution.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11529278/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142460567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DevelopmentPub Date : 2024-10-15Epub Date: 2024-10-04DOI: 10.1242/dev.203077
Kimberly L Cooper
{"title":"The case against simplistic genetic explanations of evolution.","authors":"Kimberly L Cooper","doi":"10.1242/dev.203077","DOIUrl":"10.1242/dev.203077","url":null,"abstract":"<p><p>Humans are curious to understand the causes of traits that distinguish us from other animals and that distinguish vastly different species from one another. We also have a proclivity for simple stories and sometimes tend toward seeking and accepting simple genetic explanations for large evolutionary shifts, even to a single gene. Here, I reveal how a biased expectation of mechanistic simplicity threads through the long history of evolutionary and developmental genetics. I argue, however, that expecting a simple mechanism threatens a deeper understanding of evolution, and I define the limitations for interpreting experimental evidence in evolutionary developmental genetics.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11463953/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142379204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DevelopmentPub Date : 2024-10-07DOI: 10.1242/dev.202777
Maarten Bebelman, Lenka Belicova, Elzbieta Gralinska, Tobias Jumel, Aparajita Lahree, Sarah Sommer, Andrej Shevchenko, Timofei Zatsepin, Yannis Kalaidzidis, Martin Vingron, Marino Zerial
{"title":"Hepatocyte differentiation requires anisotropic expansion of bile canaliculi.","authors":"Maarten Bebelman, Lenka Belicova, Elzbieta Gralinska, Tobias Jumel, Aparajita Lahree, Sarah Sommer, Andrej Shevchenko, Timofei Zatsepin, Yannis Kalaidzidis, Martin Vingron, Marino Zerial","doi":"10.1242/dev.202777","DOIUrl":"https://doi.org/10.1242/dev.202777","url":null,"abstract":"<p><p>During liver development, bipotential progenitor cells called hepatoblasts differentiate into hepatocytes or cholangiocytes. Hepatocyte differentiation is uniquely associated with multi-axial polarity, enabling the anisotropic expansion of apical lumina between adjacent cells and formation of a three-dimensional network of bile canaliculi (BC). Cholangiocytes, the cells forming the bile ducts, exhibit the vectorial polarity characteristic of epithelial cells. Whether cell polarization feeds back on the gene regulatory pathways governing hepatoblast differentiation is unknown. Here, we used primary hepatoblasts to investigate the contribution of anisotropic apical expansion to hepatocyte differentiation. Silencing of the small GTPase Rab35 caused isotropic lumen expansion and formation of multicellular cysts with the vectorial polarity of cholangiocytes. Gene expression profiling revealed that these cells express reduced levels of hepatocyte markers and upregulate genes associated with cholangiocyte identity. Time-course RNA sequencing demonstrated that loss of lumen anisotropy precedes these transcriptional changes. Independent alterations in apical lumen morphology induced either by modulation of the subapical actomyosin cortex or increased intraluminal pressure caused similar transcriptional changes. These findings suggest that cell polarity and lumen morphogenesis feedback to hepatoblast-to-hepatocyte differentiation.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DevelopmentPub Date : 2024-10-01Epub Date: 2024-10-14DOI: 10.1242/dev.202998
Ramiah R Vickers, Garhett L Wyatt, Lilia Sanchez, Jordyn J VanPortfliet, A Phillip West, Weston W Porter
{"title":"Loss of STING impairs lactogenic differentiation.","authors":"Ramiah R Vickers, Garhett L Wyatt, Lilia Sanchez, Jordyn J VanPortfliet, A Phillip West, Weston W Porter","doi":"10.1242/dev.202998","DOIUrl":"10.1242/dev.202998","url":null,"abstract":"<p><p>Heightened energetic and nutrient demand during lactogenic differentiation of the mammary gland elicits upregulation of various stress responses to support cellular homeostasis. Here, we identify the stimulator of interferon genes (STING) as an immune supporter of the functional development of mouse mammary epithelial cells (MECs). An in vitro model of MEC differentiation revealed that STING is activated in a cGAS-independent manner to produce both type I interferons and proinflammatory cytokines in response to the accumulation of mitochondrial reactive oxygen species. Induction of STING activity was found to be dependent on the breast tumor suppressor gene single-minded 2 (SIM2). Using mouse models of lactation, we discovered that loss of STING activity results in early involution of #3 mammary glands, severely impairing lactational performance. Our data suggest that STING is required for successful functional differentiation of the mammary gland and bestows a differential lactogenic phenotype between #3 mammary glands and the traditionally explored inguinal 4|9 pair. These findings affirm unique development of mammary gland pairs that is essential to consider in future investigations into normal development and breast cancer initiation.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11528151/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142460568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DevelopmentPub Date : 2024-10-01Epub Date: 2024-10-10DOI: 10.1242/dev.204427
{"title":"The people behind the papers - Isabella Burda and Adrienne Roeder.","authors":"","doi":"10.1242/dev.204427","DOIUrl":"https://doi.org/10.1242/dev.204427","url":null,"abstract":"<p><p>Morphogenesis in plants is often robust, resulting in a reproducible organ size and shape across organisms. In a new study, Adrienne Roeder and colleagues investigate this robustness in the developing Arabidopsis thaliana sepal. They find that the robustness is not affected by changes in the amount of cell division, but the variability of cellular growth rate must be uncorrelated or anti-correlated for robust development to occur. To find out more about the work, we caught up with first author Isabella Burda and corresponding author Adrienne Roeder, Associate Professor at Cornell University, USA.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142460569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DevelopmentPub Date : 2024-10-01Epub Date: 2024-10-10DOI: 10.1242/dev.202531
Isabella Burda, Fridtjof Brauns, Frances K Clark, Chun-Biu Li, Adrienne H K Roeder
{"title":"Robust organ size in Arabidopsis is primarily governed by cell growth rather than cell division patterns.","authors":"Isabella Burda, Fridtjof Brauns, Frances K Clark, Chun-Biu Li, Adrienne H K Roeder","doi":"10.1242/dev.202531","DOIUrl":"10.1242/dev.202531","url":null,"abstract":"<p><p>Organ sizes and shapes are highly reproducible, or robust, within a species and individuals. Arabidopsis thaliana sepals, which are the leaf-like organs that enclose flower buds, have consistent size and shape, indicating robust development. Cell growth is locally heterogeneous due to intrinsic and extrinsic noise. To achieve robust organ shape, fluctuations in cell growth must average to an even growth rate, which requires that fluctuations are uncorrelated or anti-correlated in time and space. Here, we live image and quantify the development of sepals with an increased or decreased number of cell divisions (lgo mutant and LGO overexpression, respectively), a mutant with altered cell growth variability (ftsh4), and double mutants combining these. Changes in the number of cell divisions do not change the overall growth pattern. By contrast, in ftsh4 mutants, cell growth accumulates in patches of over- and undergrowth owing to correlations that impair averaging, resulting in increased organ shape variability. Thus, we demonstrate in vivo that the number of cell divisions does not affect averaging of cell growth, preserving robust organ morphogenesis, whereas correlated growth fluctuations impair averaging.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11488635/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DevelopmentPub Date : 2024-10-01Epub Date: 2024-10-08DOI: 10.1242/dev.202694
Hyemin Min, Emily L Spaulding, Catherine S Sharp, Pankaj Garg, Esther Jeon, Lyn S Miranda Portillo, Noah A Lind, Dustin L Updike
{"title":"A role for BYN-1/bystin in cellular uptake and clearance of residual bodies in the Caenorhabditis elegans germline.","authors":"Hyemin Min, Emily L Spaulding, Catherine S Sharp, Pankaj Garg, Esther Jeon, Lyn S Miranda Portillo, Noah A Lind, Dustin L Updike","doi":"10.1242/dev.202694","DOIUrl":"10.1242/dev.202694","url":null,"abstract":"<p><p>GLH/Vasa/DDX4 helicases are core germ-granule proteins that promote germline development and fertility. A yeast-two-hybrid screen using Caenorhabditis elegans GLH-1 as bait identified BYN-1, the homolog of human bystin/BYSL. In humans, bystin promotes cell adhesion and invasion in gliomas, and, with its binding partner trophinin, triggers embryonic implantation into the uterine wall. C. elegans embryos do not implant and lack a homolog of trophinin, but both trophinin and GLH-1 contain unique decapeptide phenylalanine-glycine (FG)-repeat domains. In germ cells, we find endogenous BYN-1 in the nucleolus, partitioned away from cytoplasmic germ granules. However, BYN-1 enters the cytoplasm during spermatogenesis to colocalize with GLH-1. Both proteins become deposited in residual bodies (RBs), which are then engulfed and cleared by the somatic gonad. We show that BYN-1 acts upstream of CED-1 to drive RB engulfment, and that removal of the FG-repeat domains from GLH-1 and GLH-2 can partially phenocopy byn-1 defects in RB clearance. These results point to an evolutionarily conserved pathway whereby cellular uptake is triggered by the cytoplasmic mobilization of bystin/BYN-1 to interact with proteins harboring FG-repeats.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11488650/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DevelopmentPub Date : 2024-10-01Epub Date: 2024-10-09DOI: 10.1242/dev.203019
Theadora Tolkin, Julia Burnett, E Jane Albert Hubbard
{"title":"A role for organ level dynamics in morphogenesis of the C. elegans hermaphrodite distal tip cell.","authors":"Theadora Tolkin, Julia Burnett, E Jane Albert Hubbard","doi":"10.1242/dev.203019","DOIUrl":"10.1242/dev.203019","url":null,"abstract":"<p><p>The morphology of cells in vivo can arise from a variety of mechanisms. In the Caenorhabditis elegans hermaphrodite gonad, the distal tip cell (DTC) elaborates into a complex plexus over a relatively short developmental time period, but the mechanisms underlying this change in cell morphology are not well defined. We correlated the time of DTC elaboration with the L4-to-adult molt, but ruled out a relevant heterochronic pathway as a cue for DTC elaboration. Instead, we found that the timing of gonad elongation and aspects of underlying germline flux influence DTC elaboration. We propose a 'hitch and tow' aspect of organ-level dynamics that contributes to cellular morphogenesis, whereby germline flux drags the flexible DTC cell cortex away from its stationary cell body. More broadly, we speculate that this mechanism may contribute to cell shape changes in other contexts with implications for development and disease.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11488634/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}