向 G/S 内循环的程序性发育转换通过细胞大小的增加导致组织生长。不定期的诱导内循环细胞 (iEC) 可促进伤口愈合，但也会导致癌症。然而，关于这些 iEC 如何影响组织生长，仍有许多未知之处。使用黑腹果蝇翼盘作为模型，我们发现 iEC 群体最初大小增加，但随后经历异质停滞，导致严重的组织生长不足。 iEC 受到 DNA 损伤并激活 Jun N 末端激酶 (JNK) 通路，但与其他应激细胞不同，它具有抗凋亡能力，并且不会从上皮细胞中消除。相反，iEC 进入了 JNK 依赖性且可逆的衰老样停滞状态。衰老的 iEC 促进了二倍体邻居的分裂，但这种补偿性增殖并不能挽救组织生长。我们的研究揭示了 iEC 的独特属性及其对组织生长的影响，这对于了解它们在伤口愈合和癌症中的作用具有重要意义。版权所有：© 2024 Huang 等人。这是一篇根据知识共享署名许可条款分发的开放获取文章，允许在任何媒体上不受限制地使用、分发和复制，前提是注明原始作者和来源。

A programmed developmental switch to G / S endocycles results in tissue growth through an increase in cell size. Unscheduled, induced endocycling cells (iECs) promote wound healing but also contribute to cancer. Much remains unknown, however, about how these iECs affect tissue growth. Using the D. melanogaster wing disc as model, we find that populations of iECs initially increase in size but then subsequently undergo a heterogenous arrest that causes severe tissue undergrowth. iECs acquired DNA damage and activated a Jun N-terminal kinase (JNK) pathway, but, unlike other stressed cells, were apoptosis-resistant and not eliminated from the epithelium. Instead, iECs entered a JNK-dependent and reversible senescent-like arrest. Senescent iECs promoted division of diploid neighbors, but this compensatory proliferation did not rescue tissue growth. Our study has uncovered unique attributes of iECs and their effects on tissue growth that have important implications for understanding their roles in wound healing and cancer.Copyright: © 2024 Huang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.