• CHAP31;
  • cleavage defects;
  • colchicine;
  • embryo;
  • HDAC;
  • microtubules;
  • TSA;
  • tubacin

Volvox carteri f. nagariensis (Iyengar) possesses several thousand cells of just two types, gonida and somatic cells, that are set apart by asymmetric cell division. Because the division apparatus contains microtubules enriched in acetylated α-tubulin, we wished to know whether acetylated tubulin plays any role in regulating division symmetry. Two different human histone deacetylases (HDACs) have been shown to deacetylate tubulin in vivo, thereby regulating cell motility. Here we set out to determine: (1) whether HDAC inhibitors that increase tubulin acetylation in animal cells have the same effect in V. carteri, (2) whether increasing acetylated tubulin affects microtubule stability, and (3) whether increasing acetylated tubulin affects division symmetry. Embryos exposed to two HDAC inhibitors, trichostatin A (TSA) and tubacin, accrued dramatically higher levels of acetylated tubulin (and more acetylated microtubules) and were significantly more sensitive to colchicine than controls. However, while TSA-treated embryos cleaved aberrantly to produce adults with abnormal morphology, tubacin-treated embryos developed normally. We conclude that increasing tubulin acetylation subtly alters microtubule stability, but does not appear to affect cell division in V. carteri.