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果蝇同源异型基因变形的自催化作用和表型表达:其对极性和同源异型基因功能的依赖性

Autocatalysis and phenotypic expression of Drosophila homeotic gene Deformed: its dependence on polarity and homeotic gene function.

作者信息

González-Reyes A, Macías A, Morata G

机构信息

Centro de Biología Molecular, Universidad Autónoma de Madrid, Spain.

出版信息

Development. 1992 Dec;116(4):1059-68. doi: 10.1242/dev.116.4.1059.

Abstract

Previously published experiments have shown that the endogenous Dfd gene can be ectopically activated by its own (heat-shock-driven) product in a subset of cells of different segments. This results in the differentiation of maxillary structures like cirri and mouth hooks in places where they normally do not appear, and represents a phenomenon of autocatalysis of homeotic gene function that differs from the normal activation process. We show that this out-of-context activation occurs in cells belonging to the anterior compartments of the three thoracic and the A1 to A8 abdominal segments and that it requires the normal function of the polarity genes wingless (wg) and engrailed (en). The wg product, in addition to that of Dfd, appears to be sufficient to activate the endogenous Dfd gene in many embryonic cells. We have studied the effect of several homeotic genes on Dfd activation and phenotypic expression: Scr, Antp, Ubx and Abd-B repress Dfd both transcriptionally and at the phenotypic level, if their products are in sufficient amounts. The endogenous abd-A gene does not have a noticeable effect, but when it is replaced by an hsp70-abd-A gene, which produces a high and uniform level of expression, the phenotypic expression of Dfd is suppressed. Our results also suggest that the differentiation of cirri is induced by Dfd-expressing cells in non-expressing neighboring cells, and that this interaction occurs across the parasegmental border.

摘要

先前发表的实验表明,内源性Dfd基因可被其自身(热休克驱动)的产物在不同节段的一部分细胞中异位激活。这导致在上颌结构通常不会出现的部位分化出触须和口钩等结构,代表了一种同源异型基因功能的自催化现象,与正常激活过程不同。我们发现这种异常激活发生在三个胸段以及腹部A1至A8节段的前部区域的细胞中,并且这需要极性基因无翅(wg)和 engrailed(en)的正常功能。除了Dfd的产物外,wg产物似乎也足以在许多胚胎细胞中激活内源性Dfd基因。我们研究了几个同源异型基因对Dfd激活和表型表达的影响:如果Scr、Antp、Ubx和Abd - B的产物数量充足,它们会在转录水平和表型水平上抑制Dfd。内源性abd - A基因没有明显影响,但当它被一个能产生高水平且均匀表达的hsp70 - abd - A基因取代时,Dfd的表型表达受到抑制。我们的结果还表明,触须的分化是由表达Dfd的细胞在不表达的相邻细胞中诱导产生的,并且这种相互作用发生在副节边界上。

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