Multiple roles of the eyes absent gene in Drosophila

Multiple roles of the eyes absent gene in Drosophila
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DOI:
10.1006/dbio.1997.8845
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发表时间:
1998-04-01
影响因子:
2.7
通讯作者:
Benzer, S
Benzer, S
中科院分区:
生物学3区
文献类型:
--
作者:
Bonini, NM;Leiserson, WM;Benzer, S

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Eya基因在果蝇眼的形成过程中起着重要的作用;在视网膜祖细胞中没有Eya的表达,它们在形态发生沟之前经历程序性细胞死亡,导致无眼或减少的眼表型。因此,深入了解该基因在ny中的功能,可能与其同源基因在脊椎动物中的作用有关。在亚细胞水平的详细研究表明,Eya蛋白定位于核质,表明在控制核事件中的作用,Efa基因在眼睛以外的组织中表现出表达和作用,包括成人视觉系统、脑和卵巢的细胞亚群,以及在胚胎中的精细表达模式。epa基因的各种突变会导致单眼缺失、雌性不育或致死。胚胎致死表型的分析表明,突变等位基因显示头部形态发生的缺陷。这些数据表明,除了在早期眼睛形成中的作用外,Eya在动物中许多组织的形态发生中具有关键作用。尽管NY在多个发育阶段具有多种作用,但当在幼虫发育期间异位表达时,I型和II型蛋白质都可以指导眼的形成。(C)北京:科学出版社.
The eyes absent (eya) gene plays an essential role in the events that lead to formation of the Drosophila eye; without expression of eya in retinal progenitor cells, they undergo programmed cell death just prior to the morphogenetic furrow, leading to an eyeless or reduced eye phenotype, The eya gene has recently been found to be highly conserved to humans, defining a new gene family. Insights into the gene's function in the ny, therefore, are likely to be relevant to the role of its homologs in vertebrates. Detailed studies at the subcellular level indicate that the Eya protein is localized to the nucleoplasm, suggesting a role in control of nuclear events, The efa gene shows expression and roles in tissues other than the eye, including subsets of cells of the adult visual system, brain, and ovary, as well as an elaborate expression pattern in the embryo. Various mutations in the epa gene cause loss of ocelli, female sterility, or lethality. Analysis of the embryonic lethal phenotype indicates that mutant alleles show defects in head morphogenesis. These data indicate that eya has critical roles in morphogenesis of a number of tissues in the animal, in addition to its role in early eye formation. Despite multiple roles at multiple stages of development of the ny, both the type I and type II forms of the protein, when expressed ectopically during larval development, can direct eye formation. (C) 1998 Academic Press.