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果蝇合子致死基因穿梭载体在胚胎正常发育过程中是母源性必需的。

The Drosophila zygotic lethal gene shuttle craft is required maternally for proper embryonic development.

作者信息

Tolias P P, Stroumbakis N D

机构信息

Public Health Research Institute, 455 First Avenue, New York, NY 10016, USA.

出版信息

Dev Genes Evol. 1998 Jul;208(5):274-82. doi: 10.1007/s004270050182.

Abstract

The Drosophila gene shuttle craft (stc) is expressed zygotically in the embryonic central nervous system (CNS) where it is required to maintain the proper morphology of motoneuronal axon nerve routes following their migration from the ventral cord. Here, we report that a prominent maternal source of STC protein is also present throughout both oogenesis and embryogenesis. To determine whether this maternal component is required in the ovary and/or embryo, we used the Drosophila autosomal dominant female sterile technique to generate germ-line clones that lacked the stc maternal function. Our results demonstrate that a maternally derived source of STC protein is required during embryogenesis but not oogenesis. In contrast to the zygotic phenotype, the primary defect in embryos derived from stc germ-line clones affects segmentation by causing disruptions and deletions in distinct thoracic (T1-T3) and abdominal (A4-A8) segments. These localized defects are responsible for additional phenotypes observed later in development which include gaps in the ventral nerve cord and deletions of denticle belts in the cuticle. An additional phenotype occurring in all other neuromeric segments consists of the misguided migration of motoneuronal axons as they project out of the ventral nerve cord. Thus, the stc zygotic function is required later in development and cannot correct the segmentation and subsequent CNS abnormalities associated with loss of its earlier acting maternally derived activity.

摘要

果蝇基因穿梭载体(stc)在胚胎中枢神经系统(CNS)中合子表达,在运动神经元轴突神经通路从腹侧索迁移后,它对于维持其正常形态是必需的。在此,我们报道在整个卵子发生和胚胎发生过程中也存在显著的STC蛋白母源来源。为了确定卵巢和/或胚胎中是否需要这种母源成分,我们使用果蝇常染色体显性雌性不育技术来产生缺乏stc母源功能的生殖系克隆。我们的结果表明,胚胎发生过程中需要母源来源的STC蛋白,而卵子发生过程中则不需要。与合子表型相反,源自stc生殖系克隆的胚胎中的主要缺陷通过导致不同胸段(T1 - T3)和腹段(A4 - A8)的破坏和缺失来影响体节形成。这些局部缺陷导致了发育后期观察到的其他表型,包括腹侧神经索中的间隙和表皮中齿带的缺失。在所有其他神经节段出现的另一种表型是运动神经元轴突从腹侧神经索伸出时的错误迁移。因此,stc合子功能在发育后期是必需的,并且不能纠正与早期起作用的母源活性丧失相关的体节形成及随后的中枢神经系统异常。

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