Identifying Key Genetic Regions for Cell Sheet Morphogenesis on Chromosome 2L Using a Drosophila Deficiency Screen in Dorsal Closure.

Identifying Key Genetic Regions for Cell Sheet Morphogenesis on Chromosome 2L Using a Drosophila Deficiency Screen in Dorsal Closure.
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使用果蝇背部闭合缺陷筛选确定染色体2L上细胞片层形态发生的关键遗传区域。

DOI:
10.1534/g3.120.401386
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发表时间:
2020-11-05
期刊:
G3 (Bethesda, Md.)
影响因子:
--
通讯作者:
Kiehart DP
Kiehart DP
中科院分区:
其他
文献类型:
--
作者:
Fogerson SM;Mortensen RD;Moore RP;Chiou HY;Prabhu NK;Wei AH;Tsai D;Jadi O;Andoh-Baidoo K;Crawford J;Mudziviri M;Kiehart DP

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细胞片的形态发生对后生动物的发育和动物形态的动态平衡是必不可少的--它有助于包括原肠形成、神经管闭合、心脏和腭部形成在内的发育里程碑,以及伤口愈合期间的组织维持。背部闭合是果蝇胚胎发育的一个典型阶段,也是细胞膜形态发生的模型,是一个非常强健的过程,在这个过程中,保守的基因表达模式和信号级联调节细胞形状的变化和运动。由于成像和遗传学的进步,新的“背部闭合基因”不断被发现。在这里,我们将我们之前对第二条染色体右臂的研究扩展到第二条染色体的左臂,使用Bloomington缺陷试剂盒的一组大片段缺失,这些缺失总共移除了第二条染色体(2L)左臂98.9%的基因,以识别“背部闭合缺陷”。我们成功地筛选了87.2%的基因,在49个纯合的胚胎中鉴定出了不同的背部闭合缺陷,其中27个缺失了未知的背部闭合基因。这些纯合子缺陷导致细胞形状、眼角形成和组织动力学方面的缺陷。在这些缺陷中,我们已经确定青春痘、奇数跳过、成对和草率配对的1是2L上影响外侧表皮细胞的背部闭合基因。我们将继续通过进一步的分析来寻找新的‘背部闭合基因’。这些前向基因筛查预计将确定有助于闭合的新过程和途径,以及已知的协调闭合的各个方面的途径和结构之间的联系。
Cell sheet morphogenesis is essential for metazoan development and homeostasis of animal form – it contributes to developmental milestones including gastrulation, neural tube closure, heart and palate formation and to tissue maintenance during wound healing. Dorsal closure, a well-characterized stage in Drosophila embryogenesis and a model for cell sheet morphogenesis, is a remarkably robust process during which coordination of conserved gene expression patterns and signaling cascades regulate the cellular shape changes and movements. New ‘dorsal closure genes’ continue to be discovered due to advances in imaging and genetics. Here, we extend our previous study of the right arm of the 2nd chromosome to the left arm of the 2nd chromosome using the Bloomington deficiency kit’s set of large deletions, which collectively remove 98.9% of the genes on the left arm of chromosome two (2L) to identify ‘dorsal closure deficiencies’. We successfully screened 87.2% of the genes and identified diverse dorsal closure defects in embryos homozygous for 49 deficiencies, 27 of which delete no known dorsal closure gene. These homozygous deficiencies cause defects in cell shape, canthus formation and tissue dynamics. Within these deficiencies, we have identified pimples, odd-skipped, paired, and sloppy-paired 1 as dorsal closure genes on 2L that affect lateral epidermal cells. We will continue to identify novel ‘dorsal closure genes’ with further analysis. These forward genetic screens are expected to identify new processes and pathways that contribute to closure and links between pathways and structures already known to coordinate various aspects of closure.
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