Reference Report
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| Citation | Hanyu-Nakamura, K., Kobayashi, S., Nakamura, A. (2004). Germ cell-autonomous Wunen2 is required for germline development in Drosophila embryos. Development 131(18): 4545--4553. (Export to RIS) | ||
| FlyBase ID | FBrf0180147 | ||
| Publication Type | Research paper | ||
| PubMed ID | 15342479 | ||
| PubMed Abstract | In many animals, primordial germ cells (PGCs) migrate through the embryo towards the future gonad, a process guided by attractive and repulsive cues provided from surrounding somatic cells. In Drosophila, the two related lipid phosphate phosphatases (LPPs), Wunen (Wun) and Wun2, are thought to degrade extracellular substrates and to act redundantly in somatic cells to provide a repulsive environment to steer the migration of PGCs, or pole cells. Wun and Wun2 also affect the viability of pole cells, because overexpression of either one in somatic cells causes pole cell death. However, the means by which they regulate pole cell migration and survival remains elusive. We report that Wun2 has a maternal function required for the survival of pole cells during their migration to the gonad. Maternal wun2 RNA was found to be concentrated in pole cells and pole cell-specific expression of wun2 rescued the pole cell death phenotype of the maternal wun2 mutant, suggesting that wun2 activity in pole cells is required for their survival. Furthermore, we obtained genetic evidence that pole cell survival requires a proper balance of LPP activity in pole cells and somatic cells. We propose that Wun2 in pole cells competes with somatic Wun and Wun2 for a common lipid phosphate substrate, which is required by pole cells to produce their survival signal. In somatic cells, Wun and Wun2 may provide a repulsive environment for pole cell migration by depleting this extracellular substrate. | ||
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| Language of Publication | English | ||
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| Publication Type | Journal | ||
| Abbreviation | Development | ||
| Title | Development | ||
| Publication Year | 1987- | ||
| ISBN/ISSN | 0950-1991 | ||
Data from Reference
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Aberrations (7)
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Alleles (12)
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Constructs (7)
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Genes (10)
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