The long-term objective of this project is to understand the molecular basis for soma-germline interactions that govern germline proliferation and meiotic entry. In humans, sterility can result from insufficient proliferation of germ cells or from developmental or hormonal abnormalities that interfere with gamete production or function. Germline-based malignancy can result from over-proliferation of germ cells that retain or re-acquire mitotic potential. In many animals, early germline amplification occurs within the developing somatic gonad, and communication between the soma and germ line ensures their coordinate development. The relatively facile molecular/genetic dissection of the control of germline amplification and meiotic entry in a simple animal such as C. elegans will aid our understanding of this process in general. Recent results indicate that distinct cells in the C. elegans hermaphrodite somatic gonadal sheath lineage influence (1) germline amplification and spatio-temporal control of meiotic entry and (2) inappropriate germline tumor formation. This proposal aims to elucidate the molecular basis for each of these interactions by molecular/genetic analysis of known mutants that mimic the effect of removal of the somatic cells involved, and by genome-wide genetic screening using reverse-genetic methods that distinguish between somatic-and germline-autonomous activities.
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