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Gene Review:

mig-10 - Protein MIG-10

Caenorhabditis elegans

Manser, J. et al., Chang, C. et al., Manser, J. et al.

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High impact information on mig-10

In axons that are guided toward ventral netrin, unc-34 is required for the formation of filopodia and mig-10 increases the number of filopodia [1].
C. elegans cell migration gene mig-10 shares similarities with a family of SH2 domain proteins and acts cell nonautonomously in excretory canal development [2].
Finally, we report the results of a genetic mosaic analysis which reveal that mig-10 acts cell nonautonomously in the development of the excretory canals and suggest a possible focus for mig-10 activity within descendants of the AB cell lineage [2].
Elucidation of the role of mig-10 in C. elegans development should lead to a better understanding of cell migration and may shed light on the function of a family of SH2 domain proteins apparently involved in signal transduction and cancer [2].
All the migration phenotypes show incomplete penetrance and variable expressively, although genetic tests suggest that mutations at mig-10 and vab-8 result in complete or nearly complete loss of gene function [3].

Biological context of mig-10

The single mutants have relatively mild phenotypes, but mig-10; unc-34 double mutants arrest early in development with severe axon guidance defects [1].

References

MIG-10/lamellipodin and AGE-1/PI3K promote axon guidance and outgrowth in response to slit and netrin. Chang, C., Adler, C.E., Krause, M., Clark, S.G., Gertler, F.B., Tessier-Lavigne, M., Bargmann, C.I. Curr. Biol. (2006) [Pubmed]
C. elegans cell migration gene mig-10 shares similarities with a family of SH2 domain proteins and acts cell nonautonomously in excretory canal development. Manser, J., Roonprapunt, C., Margolis, B. Dev. Biol. (1997) [Pubmed]
Mutations affecting embryonic cell migrations in Caenorhabditis elegans. Manser, J., Wood, W.B. Dev. Genet. (1990) [Pubmed]

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