Intraflagellar transport moves proteins in and out of flagella/cilia and it is essential for the assembly of these organelles. Using whole-genome sequencing, we identified splice site mutations in two
IFT
genes,
IFT81
(
fla9
) and
IFT121
(
ift121-2
), which lead to flagellar assembly defects in the unicellular green alga
Chlamydomonas reinhardtii
. The splicing defects in these
ift
mutants are partially corrected by mutations in two conserved spliceosome proteins, DGR14 and FRA10. We identified a
dgr14
deletion mutant, which suppresses the 3′ splice site mutation in
IFT81
, and a frameshift mutant of
FRA10
, which suppresses the 5′ splice site mutation in
IFT121
. Surprisingly, we found
dgr14-1
and
fra10
mutations suppress both splice site mutations. We suggest these two proteins are involved in facilitating splice site recognition/interaction; in their absence some splice site mutations are tolerated. Nonsense mutations in
SMG1
, which is involved in nonsense-mediated decay, lead to accumulation of aberrant transcripts and partial restoration of flagellar assembly in the
ift
mutants. The high density of introns and the conservation of noncore splicing factors, together with the ease of scoring the
ift
mutant phenotype, make
Chlamydomonas
an attractive organism to identify new proteins involved in splicing through suppressor screening.
</jats:p
