Gap junctions are ubiquitous in metazoans and play critical roles in important biological processes, including electrical conduction and development. Yet, only a few defined molecules passing through gap junction channels have been linked to specific functions. We isolated gap junction channel mutants that reduce coupling between the soma and germ cells in the C. elegans gonad. We provide evidence that malonyl-CoA, the rate-limiting substrate for fatty acid synthesis (FAS), is produced in the soma and delivered through gap junctions to the germline; there it is used in fatty acid synthesis to critically support embryonic development. Separation of malonyl-CoA production from its site of utilization facilitates somatic control of germline development. Additionally, we demonstrate that loss of malonyl-CoA production in the intestine negatively impacts germline development independently of FAS. Our results suggest that metabolic outsourcing of malonyl-CoA may be a strategy by which the soma communicates nutritional status to the germline.
Bibliographical noteFunding Information:
This conclusion is supported by genetic mosaic analysis of pod-2, transformation
enthusiasm in all things concerning gap junctions. This work was supported by
We are grateful to our colleagues Gabriela Huelgas-Morales, Caroline Spike, Tatsuya Tsukamoto, and Jocelyn Shaw for discussions regarding experiments and comments on the manuscript. We thank Andy Golden for his guidance and generosity during the course of this work. We would also like to thank Ross Johnson and David Hall for many years of sharing their knowledge and enthusiasm in all things concerning gap junctions. This work was supported by National Institutes of Health (NIH) grant GM57173 to DG. This work was also supported in part by the Intramural Research Program of the National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases (XB, who is a member of Dr. Andy Golden?s laboratory). Some strains were provided by the Caenorhabditis Genetics Center, which is funded by grant P40OD010440 from the NIH Office of Research Infrastructure Programs. National Institutes of Health GM57173 David Greenstein.
National Institutes of Health (NIH) grant GM57173 to DG. This work was also
in the germline. This conclusion is supported by genetic mosaic analysis and
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PubMed: MeSH publication types
- Research Support, N.I.H., Intramural
- Journal Article
- Research Support, N.I.H., Extramural