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pubmed-article:12809605pubmed:abstractTextIn Volvox carteri adults, reproductive cells called gonidia are enclosed within a spherical monolayer of biflagellate somatic cells. Embryos must "invert" (turn inside out) to achieve this configuration, however, because at the end of cleavage the gonidia are on the outside and the flagellar ends of all somatic cells point inward. Generation of a bend region adequate to turn the embryo inside out involves a dramatic change in cell shape, plus cell movements. Here, we cloned a gene called invA that is essential for inversion and found that it codes for a kinesin localized in the cytoplasmic bridges that link all cells to their neighbors. In invA null mutants, cells change shape normally, but are unable to move relative to the cytoplasmic bridges. A normal bend region cannot be formed and inversion stops. We conclude that the InvA kinesin provides the motile force that normally drives inversion to completion.lld:pubmed
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pubmed-article:12809605pubmed:dateRevised2010-11-18lld:pubmed
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pubmed-article:12809605pubmed:articleTitleA kinesin, invA, plays an essential role in volvox morphogenesis.lld:pubmed
pubmed-article:12809605pubmed:affiliationDepartment of Biology, Washington University, St Louis, MO 63130, USA.lld:pubmed
pubmed-article:12809605pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12809605pubmed:publicationTypeResearch Support, U.S. Gov't, Non-P.H.S.lld:pubmed
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