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Finding Cures. Saving Children.
Kitagawa R: Elucidation of the Molecular Mechanisms that Link PTEN Function to the Spindle Assembly Checkpoint
We have identified a C. elegans homolog of the tumor suppressor PTEN, CePTEN, as one of the CeMAD1 interactors. CePTEN specifically coimmunoprecipitates with endogenous CeMAD1. Our extensive genetic analysis also revealed a functional link between CeMAD1 and CePTEN in nutrient signal–dependent cell cycle regulation of germ cell precursors during postembryonic development. We found that CeMAD1 is phosphorylated by Akt kinase, and this phosphorylation affects CeMAD1’s ability to bind other SAC components. We have also demonstrated that the expression of an unphosphorylated mutant CeMAD1 suppresses the defect in nutrient deprivation–induced cell cycle arrest of germ cell precursors caused by the loss of CePTEN. This finding suggests that the activity of CeMAD1 is regulated by nutrient signals, which are mediated by CePTEN and Akt kinase.
Analyzing the molecular mechanism by which CeMAD1 causes nutritional signal–induced cell cycle arrest of germ cells will help elucidate the molecular link between the Pten and SAC pathways. The Pten pathway may activate the SAC in response to nutrition deprivation via a mechanism that is distinct from that which mediates spindle damage. This investigation of the role of Pten in the SAC pathway will help increase our understanding of Pten function in maintaining genome stability. Elucidation of the molecular mechanism by which SAC regulates cell cycle progression during embryonic or postembryonic development will also shed light on the essential function of SAC components in multicellular organisms.
