Progression of Meiosis Is Coordinated by the Level and Location of MAPK Activation Via OGR-2 in .

During meiosis, a series of evolutionarily conserved events allow for reductional chromosome division, which is required for sexual reproduction. Although individual meiotic processes have been extensively studied, we currently know far less about how meiosis is regulated and coordinated. In the gonad, mitogen-activated protein kinase (MAPK) signaling drives oogenesis while undergoing spatial activation and deactivation waves. However, it is currently unclear how MAPK activation is governed and how it facilitates the progression of oogenesis. Here, we show that the () gene affects proper progression of oogenesis. Complete deletion of results in delayed meiotic entry and late spatial onset of double-strand break repair. Elevated levels of apoptosis are observed in this mutant, independent of the meiotic canonical checkpoints; however, they are dependent on the MAPK terminal member MPK-1/ERK. MPK-1 activation is elevated in diplotene in mutants and its aberrant spatial activation correlates with stages where meiotic progression defects are evident. Deletion of significantly reduces the expression of , a phosphatase reported to repress MPK-1, which is consistent with OGR-2 localization at chromatin in germ cells. We suggest that OGR-2 modulates the expression of to promote the timely progression of meiosis through MPK-1 spatial deactivation.