Tubulin Acetylation Deficiency Promotes Axonemal Turnover and Increases Cytoplasmic Microtubules

Abstract

Tubulin post-translational modifications regulate microtubule dynamics; among these, -tubulin acetylation has been linked to microtubule stability. We generated a Chlamydomonas mutant lacking the acetyltransferase TAT1, which completely abolished -tubulin K40 acetylation. Surprisingly, the lengths of normally acetylated structures, axonemes and rootlets, were largely unaffected. TAT1 localized to the flagellar tip, suggesting that it is the primary site of acetylation. Loss of acetylation caused an increase in axonemal tubulin turnover, as revealed by dikaryon-fusion assays. Unexpectedly, the tat1 mutant displayed an increased number of dynamic cytoplasmic microtubules and could regenerate long flagella after amputation, even when protein synthesis was inhibited. Despite these cytoskeletal changes, steady-state flagellar length, cell growth, and cell division remained essentially normal. These findings suggest that acetylation modulates microtubule behavior by regulating axonemal tubulin turnover and cytoplasmic microtubule dynamics, while cellular morphology is buffered against variations in microtubule content.