AI Article Synopsis

  • Drosophila female germline stem cells (GSCs) undergo asymmetric mitosis with a functional nuclear envelope, relying on a unique centrosome cycle that involves modified interactions with the nuclear lamina.
  • The protein Emerin is crucial for maintaining GSC centrosome structure, and its absence leads to excessive centrosome material retention and abnormal GSC behavior, resulting in reduced stem cell survival.
  • Interestingly, reducing centrosome material in emerin mutants can improve GSC survival and differentiation, indicating the importance of centrosome structure in preserving stem cell function.

Article Abstract

Drosophila female germline stem cells (GSCs) complete asymmetric mitosis in the presence of an intact, but permeable, nuclear envelope and nuclear lamina (NL). This asymmetric division requires a modified centrosome cycle, wherein mitotic centrosomes with mature pericentriolar material (PCM) embed in the NL and interphase centrosomes with reduced PCM leave the NL. This centrosome cycle requires Emerin, an NL protein required for GSC survival and germ cell differentiation. In emerin mutants, interphase GSC centrosomes retain excess PCM, remain embedded in the NL and nucleate microtubule asters at positions of NL distortion. Here, we investigate the contributions of abnormal interphase centrosomes to GSC loss. Remarkably, reducing interphase PCM in emerin mutants rescues GSC survival and partially restores germ cell differentiation. Direct tests of the effects of abnormal centrosomes were achieved by expression of constitutively active Polo kinase to drive enlargement of interphase centrosomes in wild-type GSCs. Notably, these conditions failed to alter NL structure or decrease GSC survival. However, coupling enlarged interphase centrosomes with nuclear distortion promoted GSC loss. These studies establish that Emerin maintains centrosome structure to preserve stem cell survival.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11586520PMC
http://dx.doi.org/10.1242/dev.204219DOI Listing

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