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Mitotic lethality prevents inflammation.
Nat Cell Biol
January 2025
Institute for Developmental Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.
Homologous recombination promotes non-immunogenic mitotic cell death upon DNA damage.
Nat Cell Biol
January 2025
Genome Integrity Unit, Children's Medical Research Institute, University of Sydney, Westmead, New South Wales, Australia.
Double-strand breaks (DSBs) can initiate mitotic catastrophe, a complex oncosuppressive phenomenon characterized by cell death during or after cell division. Here we unveil how cell cycle-regulated DSB repair guides disparate cell death outcomes through single-cell analysis of extended live imaging. Following DSB induction in S or G2, passage of unresolved homologous recombination intermediates into mitosis promotes non-immunogenic intrinsic apoptosis in the immediate attempt at cell division.
View Article and Find Full Text PDFA new Drosophila melanogaster research resource: CRISPR-induced mutations for clonal analysis of fourth chromosome genes.
G3 (Bethesda)
January 2025
School of Life Sciences, Arizona State University, Tempe, AZ 85287, USA.
As part of an ongoing effort to generate comprehensive resources for the experimental analysis of fourth chromosome genes in Drosophila melanogaster, the Fourth Chromosome Resource Project has used CRISPR mutagenesis with single guide RNAs to isolate mutations in 62 of the 80 fourth chromosome, protein-coding genes. These mutations were induced on a fourth chromosome bearing a basal FRT insertion to facilitate experimental approaches involving FLP recombinase-induced mitotic recombination. To permit straightforward comparisons among mutant stocks, most of the mutations were generated on isogenic fourth chromosomes, which were then crossed into a common genetic background.
View Article and Find Full Text PDFCentrioles play central roles in ciliogenesis and mitotic spindle assembly. Once assembled, centrioles exhibit long-term stability, a property essential for maintaining numerical control. How centriole stability is achieved and how it is lost in certain biological contexts are still not completely understood.
View Article and Find Full Text PDFLgl resets Par complex membrane loading at mitotic exit to enable asymmetric neural stem cell division.
bioRxiv
December 2024
Institute of Molecular Biology, Department of Chemistry and Biochemistry, 1229 University of Oregon, Eugene, OR 97403.
The Par complex regulates cell polarity in diverse animal cells , but how its localization is restricted to a specific membrane domain remains unclear. We investigated how the tumor suppressor Lethal giant larvae (Lgl) polarizes the Par complex in neural stem cells (NSCs or neuroblasts). In contrast to epithelial cells, where Lgl and the Par complex occupy mutually exclusive membrane domains, Lgl is cytoplasmic when the Par complex is apically polarized in NSCs.
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