细胞间相互作用涉及许多因素，这些相互作用导致细胞通过细胞竞争消除细胞，这是一种基于细胞适应性比较的体组织中细胞选择的环境依赖性过程。在这里，我们在果蝇中使用一系列基因测试来探索多效细胞因子肿瘤坏死因子⍺（TNF⍺）在Myc介导的细胞竞争（也称为Myc超级竞争或Myc细胞竞争）中的相对贡献。我们发现，在 Myc 细胞竞争过程中，需要果蝇唯一的 TNF、Eiger (Egr)、其受体 Grindelwald (Grnd/TNFR) 以及接头蛋白 Traf4 和 Traf6 来消除野生型“失败者”细胞。虽然 Egr 和 Grnd 之间的相互作用通常通过激活细胞内 Jun N 末端激酶 (JNK) 应激信号通路导致细胞死亡，但我们的实验表明，经典 JNK 信号传导的许多成分对于 Myc 细胞竞争中的细胞死亡是可有可无的，包括JNKKK Tak1、JNKK 半翅 (Hep) 和 JNK 篮 (Bsk)。我们的结果表明，Egr/Grnd 信号传导参与 Myc 细胞竞争，但其功能在很大程度上独立于 JNK 信号传导通路。© 作者 2024。由牛津大学出版社代表美国遗传学会出版。

Numerous factors have been implicated in the cell-cell interactions that lead to elimination of cells via cell competition, a context-dependent process of cell selection in somatic tissues that is based on comparisons of cellular fitness. Here we use a series of genetic tests in Drosophila to explore the relative contribution of the pleiotropic cytokine Tumor Necrosis Factor ⍺ (TNF⍺) in Myc-mediated cell competition (also known as Myc super-competition or Myc cell competition). We find that the sole Drosophila TNF, Eiger (Egr), its receptor Grindelwald (Grnd/TNFR), and the adaptor proteins Traf4 and Traf6 are required to eliminate wild-type "loser" cells during Myc cell competition. Although typically the interaction between Egr and Grnd leads to cell death by activating the intracellular Jun N-terminal Kinase (JNK) stress signaling pathway, our experiments reveal that many components of canonical JNK signaling are dispensable for cell death in Myc cell competition, including the JNKKK Tak1, the JNKK Hemipterous (Hep) and the JNK Basket (Bsk). Our results suggest that Egr/Grnd signaling participates in Myc cell competition, but functions in a role that is largely independent of the JNK signaling pathway.© The Author(s) 2024. Published by Oxford University Press on behalf of The Genetics Society of America.