Abstract

Although the precision of centriole duplication has aroused interest for over a century, its molecular mechanism remains almost entirely unknown. What proteins are required for a pre-existing centriole to induce assembly of a new centriole? One strong candidate is centrin, an EF hand-containing calcium binding protein first identified biochemically in green algae. Analysis of centrin mutants in the haploid unicellular alga Chlamydomonas (also known as ‘green yeast’ because of its powerful genetics) suggests that centrin is required for proper centriole segregation, and that defects in centrin lead to defects in centriole duplication. However, these studies leave several important questions about centrin function unanswered. First, centriole duplication still occurs in the Chlamydomonas centrin mutant, albeit to a reduced extent. Is this because the mutation, which was not a null, retains some residual centrin function, or because centrin is not strictly required for centriole duplication? Second, although the centrioles of Chlamydomonas are virtually identical to those of animal cells, is it possible that centrin might play a different role in animals?

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