The eye-antennal disc of Drosophila gives rise to numerous adult tissues, including the compound eyes, ocelli, antennae, maxillary palps and surrounding head capsule. The fate of each tissue is governed by the activity of unique gene regulatory networks (GRNs). The fate of the eye, for example, is controlled by a set of fourteen interlocking genes called the retinal determination (RD) network. Mutations within network members lead to replacement of the eyes with head capsule. Several studies have suggested that in these instances all retinal progenitor and precursor cells are eliminated via apoptosis and as a result the surrounding head capsule proliferates to compensate for retinal tissue loss. This model implies that the sole responsibility of the RD network is to promote the fate of the eye. We have re-analyzed eyes absent mutant discs and propose an alternative model. Our data suggests that in addition to promoting an eye fate the RD network simultaneously functions to actively repress GRNs that are responsible for directing antennal and head capsule fates. Compromising the RD network leads to the inappropriate expression of several head capsule selector genes such as cut, Lim1 and wingless. Instead of undergoing apoptosis, a population of mutant retinal progenitors and precursor cells adopt a head capsule fate. This transformation is accompanied by an adjustment of cell proliferation rates such that just enough head capsule is generated to produce an intact adult head. We propose that GRNs simultaneously promote primary fates, inhibit alternative fates and establish cell proliferation states.

译文

果蝇的眼触角盘会产生许多成年组织,包括复眼,ocelli,触角,上颌触角和周围的头囊。每个组织的命运受独特基因调控网络 (grn) 的活性控制。例如,眼睛的命运由一组称为视网膜测定 (RD) 网络的十四个连锁基因控制。网络成员内的突变导致用头囊代替眼睛。几项研究表明,在这些情况下,所有视网膜祖细胞和前体细胞都通过凋亡被消除,结果周围的头囊增殖以补偿视网膜组织的损失。该模型意味着RD网络的唯一责任是促进眼睛的命运。我们重新分析了没有变异盘的眼睛,并提出了另一种模型。我们的数据表明,除了促进眼睛的命运外,RD网络还同时发挥作用,积极抑制负责指导触角和头囊命运的grn。损害RD网络会导致一些头部胶囊选择基因 (例如cut,Lim1和wingless) 的不适当表达。突变的视网膜祖细胞和前体细胞群没有发生凋亡,而是采用了头囊命运。这种转化伴随着细胞增殖速率的调整,从而仅产生足够的头部囊来产生完整的成年头部。我们建议grn同时促进初级命运,抑制替代命运并建立细胞增殖状态。

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