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doi:10.1534/genetics.104.027615
A more recent version of this article appeared on March 1, 2005.
REGULAR RESEARCH PAPERS |
The LF1 Gene of Chlamydomonas reinhardtii Encodes a Novel Protein Required for Flagellar Length Control
Rachel L. Nguyen 1, Lai-Wa Tam 2 and Paul A. Lefebvre 1*
1 University of Minnesota
2 Univeersity of Minnesota
* To whom correspondence should be addressed. E-mail: pete{at}biosci.cbs.umn.edu.
Submitted on February 13, 2004
Revised on April 13, 2004
Accepted on 4 October 2004
ABSTRACT Flagellar length is tightly regulated in the biflagellate alga Chlamydomonas reinhardtii. Several genes required for control of flagellar length have been identified including LF1, a gene required to assemble normal-length flagella. The lf1 mutation causes cells to assemble extra-long flagella and to regenerate flagella very slowly after amputation. Here we describe the positional cloning and molecular characterization of the LF1 gene using a Bacterial Artificial Chromosome (BAC) library. LF1 encodes a protein of 804 amino acids with no obvious sequence homologues in other organisms. The single lf1 mutant allele is caused by a transversion that produces an amber stop at codon 87. Rescue of the lf1 phenotype upon transformation was obtained with clones containing the complete LF1 gene as well as clones that lack the last two exons of the gene, indicating that only the amino-terminal portion of the LF1 gene product (LF1p) is required for function. Although LF1 helps regulate flagellar length, the LF1p localizes almost exclusively in the cell body, with less than 1% of total cellular LF1p localizing to the flagella.
Key Words: flagellar assembly, flagellar length, positional cloning
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