AbstractSomatic cell fusion is widely studied in the filamentous fungus Neurospora crassa. The interaction of genetically identical germlings is mediated by a signaling mechanism in which the cells take turns in signal-sending and receiving. The switch between these physiological states is represented by the alternating membrane recruitment of the SO protein and the MAPK MAK-2. This dialog-like behavior is observed until the cells establish physical contact, when the cell-wall-integrity MAK-1 is recruited to the contact area to control the final steps of the cell fusion process. This work revealed, for the first-time, an additional MAK-1-function during the tropic growth phase. Specific inhibition of MAK-1 during tropic-growth resulted in disassembly of the actin-aster, and mislocalization of SO and MAK-2. Similar defects were observed after the inhibition of the Rho-GTPase RAC-1, suggesting a functional link between them, being MAK-1 upstream of RAC-1. In contrast, after inhibition of MAK-2, the actin-aster stayed intact, however, its subcellular localization became instable within the cell-membrane. Together these observations led to a new working model, in which MAK-1 promotes the formation and stability of the actin-aster, while MAK-2 controls its positionning and cell growth directionality.Summary statementThe CWI MAPK MAK-1 pathway controls actin cytoskeleton assembly at the cell tips through activation of the Rho-GTPase RAC-1 exclusively on somatic cell fusion.
Comparison of reprogramming ability of mouse ES and iPS cells measured by somatic cell fusion
