Department of Cell and Developmental Biology, University of Illinois Urbana-Champaign, Urbana, IL, 61801, USA.
Sci Rep. 2018 Mar 21;8(1):4950. doi: 10.1038/s41598-018-23093-z.
The imaginal discs of the genetically tractable model organism Drosophila melanogaster have been used to study cell-fate specification and plasticity, including homeotic changes and regeneration-induced transdetermination. The identity of the reprogramming mechanisms that induce plasticity has been of great interest in the field. Here we identify a change from antennal fate to eye fate induced by a Distal-less-GAL4 (DllGAL4) P-element insertion that is a mutant allele of Dll and expresses GAL4 in the antennal imaginal disc. While this fate change is not induced by tissue damage, it appears to be a hybrid of transdetermination and homeosis as the GAL4 expression causes upregulation of Wingless, and the Dll mutation is required for the fate change. Neither GAL4 expression nor a Dll mutation on its own is able to induce antenna-to-eye fate changes. This plasticity appears to be unique to the DllGAL4 line, possibly due to cellular stress induced by the high GAL4 expression combined with the severity of the Dll mutation. Thus, we propose that even in the absence of tissue damage, other forms of cellular stress caused by high GAL4 expression can induce determined cell fates to change, and selector gene mutations can sensitize the tissue to these transformations.
遗传上可操作的模式生物黑腹果蝇的 imaginal discs 已被用于研究细胞命运特化和可塑性,包括同源异形变化和再生诱导的转决定。诱导可塑性的重编程机制的特性在该领域引起了极大的兴趣。在这里,我们确定了由远端缺失-GAL4(DllGAL4)P 元素插入引起的从触角命运到眼睛命运的变化,该插入是 Dll 的突变等位基因,并在触角 imaginal disc 中表达 GAL4。虽然这种命运变化不是由组织损伤引起的,但它似乎是转决定和同源异形的混合,因为 GAL4 表达导致 Wingless 的上调,并且 Dll 突变对于命运变化是必需的。单独的 GAL4 表达或 Dll 突变本身都不能诱导触角到眼睛的命运变化。这种可塑性似乎仅存在于 DllGAL4 系中,可能是由于高 GAL4 表达引起的细胞应激与 Dll 突变的严重程度相结合所致。因此,我们提出,即使在没有组织损伤的情况下,高 GAL4 表达引起的其他形式的细胞应激也可以诱导已决定的细胞命运发生变化,并且选择基因突变可以使组织对这些转化敏感。