An unscheduled switch to endocycles induces a reversible senescent arrest that impairs growth of the Drosophila wing disc.
| Autor: | Huang YT; Department of Biology, Simon Cancer Center, Indiana University, Bloomington, IN 47405., Hesting LL; Department of Biology, Simon Cancer Center, Indiana University, Bloomington, IN 47405., Calvi BR; Department of Biology, Simon Cancer Center, Indiana University, Bloomington, IN 47405. |
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| Jazyk: | angličtina |
| Zdroj: | BioRxiv : the preprint server for biology [bioRxiv] 2024 Mar 14. Date of Electronic Publication: 2024 Mar 14. |
| DOI: | 10.1101/2024.03.14.585098 |
| Abstrakt: | 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. Competing Interests: Declaration of interests The authors declare no competing interests. |
| Databáze: | MEDLINE |
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