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| Description: a | Unattached kinetochores generate a ‘wait’ signal and recruit the spindleassembly checkpoint (SAC) proteins. The levels of mitotic-arrest deficient homologue-2 (MAD2) are high at unattached kinetochores (left) and moderately high at attached kinetochores in a monotelic pair (right). Under these conditions, the Aurora-B kinase concentrates at centromeres and is believed to be activated by the lack of tension between the sister chromatids. Bi-orientation depletes MAD2 (and budding uninhibited by benzimidazole (BUB)R1) from kinetochores and promotes the acquisition of tension in the centromere area, which is visualized as an increase in the inter-kinetochore distance between sister chromatids. When all chromosomes have achieved this situation, the SAC signal is extinguished and anaphase ensues thanks to the activation of separase, which removes sister-chromatid cohesion by proteolysing cohesin7. At entry into anaphase, Aurora-B is also depleted from the centromere region. b | Correct and incorrect attachments can occur during mitosis, and correction mechanisms exist to prevent incorrect chromosome inheritance, which would occur if improper attachment persisted until anaphase. Monotelic attachment is a normal condition during prometaphase before bi-orientation. In syntelic attachment, both sisters in a pair connect to the same pole. A mechanism that corrects this improper attachment depends on the Aurora-B/Ipl1 kinase. Merotelic attachment occurs quite frequently and is also corrected by the Aurora-B kinase. The SAC might be able to sense syntelic attachment, but it is unable to detect merotelic attachment. Picture Stats: Views: 1350 Filesize: 66.68kB Height: 636 Width: 912 Source: https://biology-forums.com/index.php?action=gallery;sa=view;id=1509 |