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合子基因表达和 MBT 导致的不同维度的沟形成。

Differentially-dimensioned furrow formation by zygotic gene expression and the MBT.

机构信息

Department of Biological Sciences, University of Denver, Denver, CO, United States of America.

出版信息

PLoS Genet. 2018 Jan 16;14(1):e1007174. doi: 10.1371/journal.pgen.1007174. eCollection 2018 Jan.

DOI:10.1371/journal.pgen.1007174
PMID:29337989
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5786337/
Abstract

Despite extensive work on the mechanisms that generate plasma membrane furrows, understanding how cells are able to dynamically regulate furrow dimensions is an unresolved question. Here, we present an in-depth characterization of furrow behaviors and their regulation in vivo during early Drosophila morphogenesis. We show that the deepening in furrow dimensions with successive nuclear cycles is largely due to the introduction of a new, rapid ingression phase (Ingression II). Blocking the midblastula transition (MBT) by suppressing zygotic transcription through pharmacological or genetic means causes the absence of Ingression II, and consequently reduces furrow dimensions. The analysis of compound chromosomes that produce chromosomal aneuploidies suggests that multiple loci on the X, II, and III chromosomes contribute to the production of differentially-dimensioned furrows, and we track the X-chromosomal contribution to furrow lengthening to the nullo gene product. We further show that checkpoint proteins are required for furrow lengthening; however, mitotic phases of the cell cycle are not strictly deterministic for furrow dimensions, as a decoupling of mitotic phases with periods of active ingression occurs as syncytial furrow cycles progress. Finally, we examined the turnover of maternal gene products and find that this is a minor contributor to the developmental regulation of furrow morphologies. Our results suggest that cellularization dynamics during cycle 14 are a continuation of dynamics established during the syncytial cycles and provide a more nuanced view of developmental- and MBT-driven morphogenesis.

摘要

尽管人们在研究产生质膜皱襞的机制方面做了大量工作,但对于细胞如何能够动态调节皱襞的大小,这仍是一个悬而未决的问题。在这里,我们深入描述了果蝇早期形态发生过程中体内的皱襞行为及其调节。我们表明,随着核周期的连续进行,皱襞尺寸的加深在很大程度上是由于引入了一个新的快速内陷阶段(内陷 II)。通过药理学或遗传学手段抑制合子转录来阻断中胚层转变(MBT)会导致内陷 II 的缺失,从而减少皱襞的尺寸。对产生染色体非整倍性的复合染色体的分析表明,X、II 和 III 染色体上的多个位点有助于产生不同尺寸的皱襞,我们追踪 X 染色体对皱襞伸长的贡献到 nullo 基因产物。我们进一步表明,检查点蛋白是皱襞伸长所必需的;然而,细胞周期的有丝分裂阶段对于皱襞的尺寸并不是严格确定的,因为在合胞皱襞周期进行时,有丝分裂阶段与活跃的内陷阶段脱钩。最后,我们检查了母体基因产物的周转情况,发现这对皱襞形态的发育调节贡献较小。我们的结果表明,第 14 个周期中的细胞化动力学是合胞周期中建立的动力学的延续,并为发育和 MBT 驱动的形态发生提供了更细致的观点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d44e/5786337/d8645b3ea7f2/pgen.1007174.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d44e/5786337/70cd53795e56/pgen.1007174.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d44e/5786337/c9389998fb42/pgen.1007174.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d44e/5786337/673c458946d2/pgen.1007174.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d44e/5786337/d2520fe2db04/pgen.1007174.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d44e/5786337/cb092cef523e/pgen.1007174.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d44e/5786337/3697eda16b77/pgen.1007174.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d44e/5786337/d8645b3ea7f2/pgen.1007174.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d44e/5786337/70cd53795e56/pgen.1007174.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d44e/5786337/c9389998fb42/pgen.1007174.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d44e/5786337/673c458946d2/pgen.1007174.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d44e/5786337/d2520fe2db04/pgen.1007174.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d44e/5786337/cb092cef523e/pgen.1007174.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d44e/5786337/3697eda16b77/pgen.1007174.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d44e/5786337/d8645b3ea7f2/pgen.1007174.g007.jpg

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