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PTP10D 介导的细胞竞争对于消除极性缺陷克隆并非必需。

PTP10D-mediated cell competition is not obligately required for elimination of polarity-deficient clones.

机构信息

Department of Molecular and Cell Biology, University of California-Berkeley, Berkeley, CA 94720, USA.

出版信息

Biol Open. 2022 Nov 1;11(11). doi: 10.1242/bio.059525. Epub 2022 Nov 10.

Abstract

Animal organs maintain tissue integrity and ensure removal of aberrant cells through several types of surveillance mechanisms. One prominent example is the elimination of polarity-deficient mutant cells within developing Drosophila imaginal discs. This has been proposed to require heterotypic cell competition dependent on the receptor tyrosine phosphatase PTP10D within the mutant cells. We report here experiments to test this requirement in various contexts and find that PTP10D is not obligately required for the removal of scribble (scrib) mutant and similar polarity-deficient cells. Our experiments used identical stocks with which another group can detect the PTP10D requirement, and our results do not vary under several husbandry conditions including high and low protein food diets. Although we are unable to identify the source of the discrepant results, we suggest that the role of PTP10D in polarity-deficient cell elimination may not be absolute.

摘要

动物器官通过几种类型的监测机制来维持组织完整性并确保清除异常细胞。一个突出的例子是,在发育中的果蝇翅盘中消除极性缺失的突变细胞。据推测,这需要依赖于突变细胞内的受体酪氨酸磷酸酶 PTP10D 的异型细胞竞争。我们在这里报告了在各种情况下测试这一要求的实验,发现 PTP10D 并非 scribble(scrib)突变和类似的极性缺失细胞清除所必需的。我们的实验使用了与另一个小组可以检测到 PTP10D 需求的相同品系,并且我们的结果在包括高蛋白和低蛋白饮食在内的几种饲养条件下都没有变化。尽管我们无法确定产生差异结果的原因,但我们认为 PTP10D 在极性缺失细胞消除中的作用可能不是绝对的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8720/9672856/fecc303c37b9/biolopen-11-059525-g1.jpg

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