Institute for Research in Immunology and Cancer, Université de Montréal, Montréal, Quebec, Canada.
Published: June 2022
AI Article Synopsis
Article Abstract
At mitotic entry, reorganization of the actomyosin cortex prompts cells to round-up. Proteins of the ezrin, radixin, and moesin family (ERM) play essential roles in this process by linking actomyosin forces to the plasma membrane. Yet, the cell-cycle signal that activates ERMs at mitotic entry is unknown. By screening a compound library using newly developed biosensors, we discovered that drugs that disassemble microtubules promote ERM activation. We further demonstrated that disassembly of interphase microtubules at mitotic entry directs ERM activation and metaphase cell rounding through GEF-H1, a Rho-GEF inhibited by microtubule binding, RhoA, and its kinase effector SLK. We finally demonstrated that GEF-H1 and Ect2, another Rho-GEF previously identified to control actomyosin forces, act together to drive activation of ERMs and cell rounding in metaphase. In summary, we report microtubule disassembly as a cell-cycle signal that controls a signaling network ensuring that actomyosin forces are efficiently integrated at the plasma membrane to promote cell rounding at mitotic entry.
Quiescence in is a reversible G crucial for long-term survival under nutrient-deprived conditions. During quiescence, the genome is hypoacetylated and chromatin undergoes significant compaction. However, the 3D structure of the ribosomal DNA (rDNA) locus in this state is not well understood.
Unlabelled: Human papillomaviruses (HPVs) travel from the trans-Golgi network (TGN) to the condensed (mitotic) chromosomes during mitosis. Partially uncoated HPV capsids utilize a unique vesicular structure for trafficking and nuclear import, which is directed by the minor capsid protein L2. However, it is still unknown which precise factors facilitate post-TGN HPV trafficking to the nucleus.
The Hippo pathway is a critical regulator of animal development. Activation of the Hippo pathway causes a cascade of phosphorylation events that culminate in the phosphorylation of the transcriptional co-factors YAP and TAZ, which limits their entry into the nucleus. When the Hippo pathway is 'off', however, YAP and TAZ can enter the nucleus, where they interact with the transcription factors of the TEA Domain (TEAD) family to regulate transcriptional activity.
Aurora kinases (AURK) play a central role in controlling cell cycle in a wide range of organisms. They belong to the family of serine-threonine kinase proteins. Their role in the cell cycle includes, among others, the entry into mitosis, maturation of the centrosome and formation of the mitotic spindle.
Genomic structural variants (SVs) significantly affect human health, yet the processes behind the formation of large, nonrecurrent changes remain largely unclear.
Common fragile sites (CFSs) serve as a model for studying SV formation, particularly large deletions, under conditions of replication stress.
Research shows that SV junctions accumulate at a higher rate during cell division (M-phase) and primarily involve a specific DNA repair process driven by DNA polymerase theta (POLQ), rather than relying on traditional mitotic DNA synthesis methods.
