Flagellar Elongation and Gene Expression inChlamydomonas reinhardtii

Lithium (Li(+)) affects the physiology of cells from a broad range of organisms including plants and both vertebrate and invertebrate animals. Although its effects result presumably from changes in gene expression elicited by its interaction with intracellular signal transduction pathways, the molecular mechanisms of Li(+) action are not well understood. The biflagellate green alga Chlamydomonas reinhardtii is an ideal genetic model for the integration of the effects on Li(+) on signal transduction, gene expression, and aspects of flagellar biogenesis. Li(+) causes C. reinhardtii flagella to elongate to approximately 1.4 times their normal length and blocks flagellar motility (S. Nakamura, H. Tabino, and M. K. Kojima, Cell Struct. Funct. 12:369-374, 1987). We report here that Li(+) treatment increases the abundance of several flagellar mRNAs, including alpha- and beta-tubulin and pcf3-21. Li(+)-induced flagellar gene expression occurs in cells pretreated with cycloheximide, suggesting that the abundance change is a response that does not require new protein synthesis. Deletion analysis of the flagellar alpha1-tubulin gene promoter showed that sequences necessary for Li(+)-induced expression differed from those for acid shock induction and contain a consensus binding site for CREB/ATF and AP-1 transcription factors. These studies suggest potential promoter elements, candidate factors, and signal transduction pathways that may coordinate the C. reinhardtii cellular response to Li(+).