Chlamydomonas Genetics Center, Duke University, 1982

Phenotype: requires acetate (probably suppressed)

Derived from CC-705 ac46 mt+ x CC-1095 fsr1 mt-.

The ac46 mutation is notoriously prone to acquire second-site suppressors. In our experience it can always be recovered by out-crossing.


  • Locus:
  • AC46 [MDH1]
  • Chromosome:
  • 15

Chlamydomonas Genetics Center, Duke University, 1982

Phenotype: antibiotic and inhibitor resistant (erythromycin, methionine sulfoximine); yellow in the dark

From a series of crosses in 1982 ending with a cross of CC-1366 ac20 y6 mt+ to CC-1105 ery3 msr1 sr1 mt-. This strain has the wild type alleles at the ac20 and sr1 loci.

This is a triply marked strain for linkage group I.


  • Locus:
  • ERY3, MSR1, Y6
  • Chromosome:
  • 1

Chlamydomonas Genetics Center, Duke University, 1982

Phenotype: antibiotic resistant (erythromycin); motility impaired

From a cross of CC-951 ac17 ery1c pf2 to CC-124 wild type.

This strain marks the centromere and right arm of linkage group XI.

For more information on the ERY1 locus, please see CC-504.


  • Locus:
  • ERY1 [PRPL4], PF2
  • Chromosome:
  • 11

Chlamydomonas Genetics Center, Duke University, 1982

Phenotype: cold sensitive on minimal medium; yellow in the dark

From CC-1171 y6 mt+ x CC-43 ac20 mt-, 1982

The ac20 y6 double mutant is intensely yellow in the dark, much more so than the y6 mutant alone.


  • Locus:
  • AC20, Y6
  • Chromosome:
  • 1

From Ralph Lewin, Scripps Institution of Oceanography, October 1982

Phenotype: impaired flagellar autotomy

The fa1 mutant was isolated by Lewin and Burrascano after UV mutagenesis, and characterized as a mutant that does not shed its flagella under conditions such as pH shock, treatment with ethanol, etc. Further analysis by Finst et al. showed that the defect is specifically in severing outer doublets of the microtubules in response to calcium, and that the corresponding gene is a novel 171-kD protein.


Lewin R and Burrascano C (1983) Another new kind of Chlamydomonas mutant, with impaired flagellar autotomy. Experientia 39:1397-1398

Quarmby LM (1996) Ca2+ influx activated by low pH in Chlamydomonas. J Gen Physiol 108:351-361

Evans JH and Keller LR (1997) Receptor-Mediated Calcium Influx in Chlamydomonas reinhardtii. J. Euk Microbiol 44:237-245

Yueh YG, Crain RC (1993) Deflagellation of Chlamydomonas reinhardtii follows a rapid transitory accumulation of inositol 1,4,5-trisphosphate and requires Ca2+ entry. J Cell Biol 123:869-875

Cheshire JL, Evans JH, Keller LR (1994) Ca2+ signaling in the Chlamydomonas flagellar regeneration system: cellular and molecular responses. J Cell Sci 107:2491-2498

Crain RC, Yueh YG (1995) Phosphoinositide signalling in plant and algal responses to physiological stimuli. Biochem Soc Trans 23:853-856

Hayashi M, Yagi T, Yoshimura K, Kamiya R (1998) Real-time observation of Ca2+-induced basal body reorientation in Chlamydomonas. Cell Motil Cytoskeleton 41:49-56

Tuxhorn J, Daise T, Dentler WL (1998) Regulation of flagellar length in Chlamydomonas. Cell Motil Cytoskeleton 40:133-146

Finst RJ, Kim PJ, Quarmby LM (1998) Genetics of the deflagellation pathway in Chlamydomonas. Genetics 149:927-936

Finst RJ, Kim PJ, Griffis ER, Quarmby LM (2000) Fa1p is a 171 kDa protein essential for axonemal microtubule severing in Chlamydomonas. J Cell Sci 113:1963-1971

Hayashi M, Yanagisawa HA, Hirono M, Kamiya R (2002) Rescue of a Chlamydomonas inner-arm-dynein-deficient mutant by electroporation-mediated delivery of recombinant p28 light chain. Cell Motil Cytoskeleton 53:273-280


  • Locus:
  • FA1
  • Chromosome:
  • 6

From Ralph Lewin, Scripps Institution of Oceanography, October 1982

Lewin sent this as gf-1. To the best of our knowledge, this is the same mutation as fg-1 (see CC-1838).

From Sammlung von Algenkulturen (SAG), December 1982

This is the type strain for C. smithii as described by Hoshaw and Ettl, who reviewed the remains of G.M. Smith’s collection after his death. It was designated 136f by Smith, and came from a sample collected in 1945 in South Deerfield, Massachusetts. Smith had paired this with another strain from California (formerly CC-1372, which is no longer in the Chlamydomonas Resource Center collection), and had identified both as C. reinhardtii. Hoshaw and Ettl concluded that these strains differed sufficiently from the laboratory strain of C. reinhardtii on morphological criteria to warrant description as a new species.

Subsequent work has shown that CC-1373 is fully fertile with C. reinhardtii, but has significant sequence polymorphisms in nuclear, chloroplast and mitochondrial DNA. CC-1372 on the other hand appears to be an unrelated homothallic strain, probably C. culleus.

This strain can grow on nitrate.

We recommend CC-1373 as a polymorphic strain for comparison with C. reinhardtii. Its one drawback is that it sometimes forms “clumpy” cultures as a result of failure of the mother cell walls to lyse after vegetative division. This property may result in poor mating efficiency. In our experience, letting the gamete mixture sit for 24 hours or more usually produces enough release of autolysin to overcome the hatching defect.

For an alternative polymorphic strain for nuclear DNA, see CC-2290, the Minnesota mt- isolate described by Gross et al. Less well characterized, but also of possible utility, are CC-2931 and CC-2932, a pair of strains isolated in North Carolina.


Hoshaw R and Ettl H (1966) A Chlamydomonad interfertile with Chlamydomonas reinhardtip. J Phycol 2:93-96

Coleman AW, Mai JC (1997) Ribosomal DNA ITS-1 and ITS-2 sequence comparisons as a tool for predicting genetic relatedness. J Mol Evol 45:168-177

Pröschold T, Harris EH, Coleman AW (2005) Portrait of a species: Chlamydomonas reinhardtii. Genetics 170:1601-1610

From Sammlung von Algenkulturen (SAG), December 1982

This strain was listed by SAG as “French isolate G. Paris 170″, implying a European origin, and was obtained by the Chlamydomonas Genetics Center for comparison with other presumptive field isolates. Ferris (1989) found however that the Gulliver transposon pattern is like that of the laboratory strains of C. reinhardtii. It did not form zygotes when tested with either CC-124 or CC-125; Ferris thinks it may be a non-mating mutant of a strain equivalent to CC-1010 or UTEX 90.


Ferris PJ (1989) Characterization of a Chlamydomonas transposon, Gulliver, resembling those in higher plants. Genetics 122:363-377

Boynton-Gillham laboratory, Duke University, 1982

Phenotype: requires acetate

This strain is a mt+ derivative, obtained by successive crosses to CC-125 wild type of a mutant isolated in a diploid strain. This strain is not arginine-requiring. The mutant shows symmetrical 9 kb deletions in both copies of the psbA gene.

This mutant was isolated in an arg2/arg7 diploid strain by Doug Rabert in 1979. Cells were pregrown in 0.5 mM 5-fluorodeoxyuridine in liquid cultures, concentrated, and irradiated with 2 minutes X-ray @ 6 krad/min. The irradiated cells were plated on 2 mM arsenate and arsenate-tolerant (non-photosynthesizing) clones were selected.


Myers AM, Grant DM, Rabert DK, Harris EH, Boynton JE, Gillham NW (1982) Mutants of Chlamydomonas reinhardtii with physical alterations in their chloroplast DNA. Plasmid 7:133-151


  • Locus:
  • psbA
  • Chromosome:
  • chloroplast

Chlamydomonas Genetics Center, Duke University 1982

Phenotype: requires acetate

This mutant came from a mutagenesis experiment by Gillham using 5-fluorodeoxyuridine treatment to generate chloroplast mutations. However, this isolate showed 2:2 inheritance in a cross to wild type, and all ac progeny were mt-, suggesting close linkage to the mating type locus.

This mutation acquires suppressors easily. All suppressors isolated thus far have been unlinked to the original mutation.


  • Locus:
  • AC213
  • Chromosome:
  • 6

From David Luck, Rockefeller University, February 1983, his isolation number ncs-26

Phenotype: impaired motility

The pf22 mutants partially lack outer dynein arms of axonemal doublet microtubules. Flagella are short in exponentially growing cells, about two-thirds of wild type length at stationary phase. For additional information on the PF22 locus, please see CC-2495.


  • Locus:
  • PF22
  • Chromosome:
  • 1

From David Luck, Rockefeller University, February 1983, his isolation number ncs-72

Phenotype: impaired motility

Mutants at the PF23 locus have flagella that are shorter than normal, and lack inner dynein arms. Please see CC-2494 for more information on this locus.


  • Locus:
  • PF23
  • Chromosome:
  • 11

From David Luck, Rockefeller University, February 1983, his isolation number ncs-3

Phenotype: impaired motility

This mutant, which was nitrosoguanidine-induced in Luck’s laboratory, partially lacks radial spokes. Seven radial spoke polypeptides are missing or reduced in quantity. Yang et al. identified the corresponding gene as RSP2.


Huang B, Piperno G, Ramanis Z, Luck DJ (1981) Radial spokes of Chlamydomonas flagella: genetic analysis of assembly and function. J Cell Biol 88:80-88

Curry AM, Rosenbaum JL (1993) Flagellar radial spoke: a model molecular genetic system for studying organelle assembly. Cell Motil Cytoskeleton 24:224-232

Yang P, Yang C, Sale WS (2004) Flagellar radial spoke protein 2 is a calmodulin binding protein required for motility in Chlamydomonas reinhardtii. Eukaryot Cell 3:72-81


  • Locus:
  • PF24 [RSP2]
  • Chromosome:
  • 10

From David Luck, Rockefeller University, February 1983, his isolation number ddm-100

Phenotype: impaired motility

Huang et al. reported that cells of pf25 mutants appear wild type in EM, but are missing one polypeptide of the radial spoke system and are deficient in another. They swim actively, but abnormally. This locus has been shown to correspond to the gene encoding the spoke stalk protein RSP11.


Huang B, Piperno G, Ramanis Z, Luck DJ (1981) Radial spokes of Chlamydomonas flagella: genetic analysis of assembly and function. J Cell Biol 88:80-88

Yang C, Yang P (2006) The flagellar motility of Chlamydomonas pf25 mutant lacking an AKAP-binding protein is overtly sensitive to medium conditions. Mol Biol Cell. 17:227-238

Yang P, Diener DR, Yang C, Kohno T, Pazour GJ, Dienes JM, Agrin NS, King SM, Sale WS, Kamiya R, Rosenbaum JL, Witman GB (2006) Radial spoke proteins of Chlamydomonas flagella. J Cell Sci 119:1165-1174


  • Locus:
  • PF25 [RSP11]
  • Chromosome:
  • 10

From David Luck, Rockefeller University, February 1983, his isolation number ts-16-2

Phenotype: impaired motility

This is currently the only pf26 strain in the collection. This locus is very closely linked to PF1, but the original pf26 mutant complements with pf1 in a stable diploid strain. The PF26 locus has been shown to correspond to the gene encoding radial spoke protein 6.


Huang B, Piperno G, Ramanis Z, Luck DJ (1981) Radial spokes of Chlamydomonas flagella: genetic analysis of assembly and function. J Cell Biol 88:80-88

Curry AM, Williams BD, Rosenbaum JL (1992) Sequence analysis reveals homology
between two proteins of the flagellar radial spoke. Mol Cell Biol 12:3967-77

Curry AM, Rosenbaum JL (1993) Flagellar radial spoke: a model molecular genetic system for studying organelle assembly. Cell Motil Cytoskeleton 24:224-232

Frey E, Brokaw CJ, Omoto CK (1997) Reactivation at low ATP distinguishes among classes of paralyzed flagella mutants. Cell Motil Cytoskeleton 38:91-99


  • Locus:
  • PF26 [RSP6]
  • Chromosome:
  • 5

From David Luck, Rockefeller University, February 1983, his isolation number ncs-83

Phenotype: impaired motility

In pf27 cells, several polypeptides associated with radial spokes are not phosphorylated, but dikaryon rescue experiments suggest that the product of the PF27 locus is not actually a radial spoke component.

This mutant is non-motile and easy to score, and is a good marker for the centromere of linkage group XII/XIII.


Huang B, Piperno G, Ramanis Z, Luck DJ (1981) Radial spokes of Chlamydomonas flagella: genetic analysis of assembly and function. J Cell Biol 88:80-88

Curry AM, Rosenbaum JL (1993) Flagellar radial spoke: a model molecular genetic system for studying organelle assembly. Cell Motil Cytoskeleton 24:224-232

Frey E, Brokaw CJ, Omoto CK (1997) Reactivation at low ATP distinguishes among classes of paralyzed flagella mutants. Cell Motil Cytoskeleton 38:91-99

Yang C, Yang P (2006) The flagellar motility of Chlamydomonas pf25 mutant lacking an AKAP-binding protein is overtly sensitive to medium conditions. Mol Biol Cell 17:227-238


  • Locus:
  • PF27
  • Chromosome:
  • 12

From David Luck, Rockefeller University, February 1983

Phenotype: variable number of flagella; abnormal cell shape; abnormal cell division

Mutants at the VFL1 locus typically have between 0 and 4 flagella, sometimes as many as 10. Cell size and shape are often abnormal, probably as a result of unequal cell divisions.. Flagellar assembly continues throughout the G1 portion of the cell cycle. This feature is unique to vfl cells.

Flagella can appear at any site on the cell surface, and there may be defects in the flagellar apparatus, including missing or defective striated fibers and reduced numbers of rootlet microtubules. Wright et al. determined that, in contrast to vfl2 mutants, vfl1 has normal levels of centrin and a stable nucleus-basal body connector.


Adams GM, Wright RL, Jarvik JW (1985) Defective temporal and spatial control of flagellar assembly in a mutant of Chlamydomonas reinhardtii with variable flagellar number. J Cell Biol 100:955-964

Wright RL, Adler SA, Spanier JG, Jarvik JW (1989) Nucleus-basal body connector in Chlamydomonas: evidence for a role in basal body segregation and against essential roles in mitosis or in determining cell polarity. Cell Motil Cytoskeleton 14:516-526

Tam LW, Lefebvre PA (1993) Cloning of flagellar genes in Chlamydomonas reinhardtii by DNA insertional mutagenesis. Genetics 135:375-384

Silflow CD, LaVoie M, Tam LW, Tousey S, Sanders M, Wu W, Borodovsky M, Lefebvre PA (2001) The Vfl1 Protein in Chlamydomonas localizes in a rotationally asymmetric pattern at the distal ends of the basal bodies. J Cell Biol 153:63-74


  • Locus:
  • VFL1
  • Chromosome:
  • 8

From David Luck, Rockefeller University, February 1983

Phenotype: impaired motility

This locus appears to be linked to FLA2, but not on linkage group IX as previously reported. The fla1 mutant fails to assemble flagella at 34 degrees. This is the original fla1 mutant. Several allelic mutants were later identified by Iomini et al.


Huang B, Rifkin MR, Luck DJ (1977) Temperature-sensitive mutations affecting flagellar assembly and function in Chlamydomonas reinhardtii. J Cell Biol 72:67-85

Adams GM, Huang B, Luck DJ (1982) Temperature-Sensitive, Assembly-Defective Flagella Mutants of CHLAMYDOMONAS REINHARDTII. Genetics 100:579-586

Iomini C, Babaev-Khaimov V, Sassaroli M, Piperno G (2001) Protein particles in Chlamydomonas flagella undergo a transport cycle consisting of four phases. J Cell Biol 153:13-24

From David Luck, Rockefeller University, February 1983

Phenotype: impaired motility

This locus appears to be linked to FLA1, but not on linkage group IX as previously reported. The fla2 mutant does not assemble flagella at 34 degrees, and flagella previously formed become unstable at this temperature. This mutation affects retrograde intraflagellar transport.


Huang B, Rifkin MR, Luck DJ (1977) Temperature-sensitive mutations affecting flagellar assembly and function in Chlamydomonas reinhardtii. J Cell Biol 72:67-85

Adams GM, Huang B, Luck DJ (1982) Temperature-Sensitive, Assembly-Defective Flagella Mutants of CHLAMYDOMONAS REINHARDTII. Genetics 100:579-586

Iomini C, Babaev-Khaimov V, Sassaroli M, Piperno G (2001) Protein particles in Chlamydomonas flagella undergo a transport cycle consisting of four phases. J Cell Biol 153:13-24

Iomini C, Li L, Esparza JM, Dutcher SK (2009) Retrograde intraflagellar transport mutants identify complex A proteins with multiple genetic interactions in Chlamydomonas reinhardtii. Genetics 183:885-896

From David Luck, Rockefeller University, February 1983

The fla3 mutant shows abnormalities in flagellar assembly at 21 degrees, and loses its flagella at 34 degrees. This is the original fla3 mutant. Iomini et al. reported in 2001 that their stock had lost its phenotype and excluded it from their further analysis. Mueller et al. also found that CC-1391 no longer had a clear temperature-sensitive phenotype, but were able to recover a good isolate from a backcross to 21 gr (CC-1690). One progeny clone from this cross (1B) was designated as fla3-1, and is now the representative allele for this mutation (see CC-4283). Mueller et al. showed that this is a mutation in the nonmotor subunit of Kinesin-2, a component of the anterograde intraflagellar transport complex.


Huang B, Rifkin MR, Luck DJ (1977) Temperature-sensitive mutations affecting flagellar assembly and function in Chlamydomonas reinhardtii. J Cell Biol 72:67-85

Adams GM, Huang B, Luck DJ (1982) Temperature-Sensitive, Assembly-Defective Flagella Mutants of CHLAMYDOMONAS REINHARDTII. Genetics 100:579-586

Iomini C, Babaev-Khaimov V, Sassaroli M, Piperno G (2001) Protein particles in Chlamydomonas flagella undergo a transport cycle consisting of four phases. J Cell Biol 153:13-24

Mueller J, Perrone CA, Bower R, Cole DG, Porter ME (2005) The FLA3 KAP subunit is required for localization of kinesin-2 to the site of flagellar assembly and processive anterograde intraflagellar transport. Mol Biol Cell 16:1341-1354


  • Locus:
  • FLA3
  • Chromosome:
  • 10

From David Luck, Rockefeller University, February 1983

Phenotype: impaired motility

The fla4 mutant fails to assemble flagella at 34 degrees. The FLA4 locus was mapped close to FLA3 on chromosome 10, but Mueller et al. found fla4 showed no alterations in the KAP gene, site of the fla3 mutation, and they were unable to rescue fla4 with a BAC clone containing the wild-type KAP gene.


Huang B, Rifkin MR, Luck DJ (1977) Temperature-sensitive mutations affecting flagellar assembly and function in Chlamydomonas reinhardtii. J Cell Biol 72:67-85

Adams GM, Huang B, Luck DJ (1982) Temperature-Sensitive, Assembly-Defective Flagella Mutants of CHLAMYDOMONAS REINHARDTII. Genetics 100:579-586

Iomini C, Babaev-Khaimov V, Sassaroli M, Piperno G (2001) Protein particles in Chlamydomonas flagella undergo a transport cycle consisting of four phases. J Cell Biol 153:13-24

Mueller J, Perrone CA, Bower R, Cole DG, Porter ME (2005) The FLA3 KAP subunit is required for localization of kinesin-2 to the site of flagellar assembly and processive anterograde intraflagellar transport. Mol Biol Cell 16:1341-1354


  • Locus:
  • FLA4
  • Chromosome:
  • 10

From David Luck, Rockefeller University, February 1983

Phenotype: impaired motility

The fla5 mutant fails to assemble flagella at 34 degrees and appears to have a deficiency in intraflagellar transport.


Adams GM, Huang B, Luck DJ (1982) Temperature-Sensitive, Assembly-Defective Flagella Mutants of CHLAMYDOMONAS REINHARDTII. Genetics 100:579-586

Iomini C, Babaev-Khaimov V, Sassaroli M, Piperno G (2001) Protein particles in Chlamydomonas flagella undergo a transport cycle consisting of four phases. J Cell Biol 153:13-24


  • Locus:
  • FLA5
  • Chromosome:
  • 11

From David Luck, Rockefeller University, February 1983, his isolation number 519

The original fla6 mutant failed to assemble flagella at 34 degrees. Iomini et al. reported that their isolate of this strain had lost its phenotype and that they were unable to analyze it further.


Adams GM, Huang B, Luck DJ (1982) Temperature-Sensitive, Assembly-Defective Flagella Mutants of CHLAMYDOMONAS REINHARDTII. Genetics 100:579-586

Iomini C, Babaev-Khaimov V, Sassaroli M, Piperno G (2001) Protein particles in Chlamydomonas flagella undergo a transport cycle consisting of four phases. J Cell Biol 153:13-24


  • Locus:
  • FLA6
  • Chromosome:
  • 6

From David Luck, Rockefeller University, February 1983, as fla7 isolation # 519.

Phenotype: impaired motility

This mutant was originally mapped in Luck’s laboratory to linkage group IV, based on limited tetrad analysis, but subsequently was found to be an allele of fla10 on linkage group XIX (chromosome 17; see Lux and Dutcher, 1991). Please see CC-1919 for more information on the FLA10 locus).

The original fla7 mutant was isolated in an ery10 background (see CC-70). We don’t know if this strain is resistant to erythromycin.


Adams GM, Huang B, Luck DJ (1982) Temperature-Sensitive, Assembly-Defective Flagella Mutants of CHLAMYDOMONAS REINHARDTII. Genetics 100:579-586

Lux FG 3rd, Dutcher SK (1991) Genetic interactions at the FLA10 locus: suppressors and synthetic phenotypes that affect the cell cycle and flagellar function in Chlamydomonas reinhardtii. Genetics 128:549-561

Miller MS, Esparza JM, Lippa AM, Lux FG 3rd, Cole DG, Dutcher SK (2005) Mutant kinesin-2 motor subunits increase chromosome loss. Mol Biol Cell 16:3810-3820

Iomini C, Li L, Esparza JM, Dutcher SK (2009) Retrograde intraflagellar transport mutants identify complex A proteins with multiple genetic interactions in Chlamydomonas reinhardtii. Genetics 183:885-896


  • Locus:
  • FLA10 [KHP1]
  • Chromosome:
  • 17

From David Luck, Rockefeller University, February 1983, his isolation number 523

Phenotype: impaired motility

The fla8 mutant fails to assemble flagella at 34 degrees. Miller et al. showed that fla8 is a m mutation in the gene encoding one of the motor subunits of kinesin-2.


Adams GM, Huang B, Luck DJ (1982) Temperature-Sensitive, Assembly-Defective Flagella Mutants of CHLAMYDOMONAS REINHARDTII. Genetics 100:579-586

Miller MS, Esparza JM, Lippa AM, Lux FG 3rd, Cole DG, Dutcher SK (2005) Mutant kinesin-2 motor subunits increase chromosome loss. Mol Biol Cell 16:3810-3820


  • Locus:
  • FLA8
  • Chromosome:
  • 12

From David Luck, Rockefeller University, February 1983, his isolation number pf6R6

This is the original sup-pf1 allele described by Huang et al. as R6, a suppressor of pf6. It was characterized as a mutation in the spoke specific suppressor system, which restores motility to radial spoke- and central-pair defective mutants without altering spoke or central pair defects. It was subsequently shown to be an allele at the ODA4 locus, corresponding to the gene encoding the beta heavy chain of the outer dynein arm.


Huang B, Ramanis Z, Luck DJ (1982) Suppressor mutations in Chlamydomonas reveal a regulatory mechanism for Flagellar function. Cell 28:115-124

Porter ME, Knott JA, Gardner LC, Mitchell DR, Dutcher SK (1994) Mutations in the SUP-PF-1 locus of Chlamydomonas reinhardtii identify a regulatory domain in the beta-dynein heavy chain. J Cell Biol 126:1495-1507

Sakato M, King SM (2003) Calcium regulates ATP-sensitive microtubule binding by Chlamydomonas outer arm dynein. J Biol Chem 278:43571-43579

Mitchell BF, Grulich LE, Mader MM (2004) Flagellar quiescence in Chlamydomonas: Characterization and defective quiescence in cells carrying sup-pf-1 and sup-pf-2 outer dynein arm mutations. Cell Motil Cytoskeleton 57:186-196


  • Locus:
  • SUP-PF1 [DHC14]
  • Chromosome:
  • 9

From David Luck, Rockefeller University, February 1983 his isolation number ncs-3R4

The sup-pf2 mutant was isolated in a pf24 strain by Huang et al., and was originally characterized as a mutation in the spoke specific suppressor system, which restores motility to radial spoke- and central-pair defective mutants without altering spoke or central pair defects. It was subsequently shown to be an allele at the ODA2 locus, corresponding to the gene encoding the gamma heavy chain of the outer dynein arm.

To the best of our knowledge, this is the original sup-pf2 allele.


Huang B, Ramanis Z, Luck DJ (1982) Suppressor mutations in Chlamydomonas reveal a regulatory mechanism for Flagellar function. Cell 28:115-124

Brokaw CJ, Luck DJ, Huang B (1982) Analysis of the movement of Chlamydomonas flagella:" the function of the radial-spoke system is revealed by comparison of wild-type and mutant flagella. J Cell Biol 92:722-732

Rupp G, O'Toole E, Gardner LC, Mitchell BF, Porter ME (1996) The sup-pf-2 mutations of Chlamydomonas alter the activity of the outer dynein arms by modification of the gamma-dynein heavy chain. J Cell Biol 135:1853-1865

Mitchell BF, Grulich LE, Mader MM (2004) Flagellar quiescence in Chlamydomonas: Characterization and defective quiescence in cells carrying sup-pf-1 and sup-pf-2 outer dynein arm mutations. Cell Motil Cytoskeleton 57:186-196


  • Locus:
  • SUP-PF2 [DHC15]
  • Chromosome:
  • 11,

From David Luck, Rockefeller University, February 1983 his isolation number pf1R62

The sup-pf3 mutation restores motility to radial spoke-defective mutants without altering spoke defects. This is an allele at the PF2 locus, which encodes component DRC4 of the dynein regulatory complex.


Huang B, Ramanis Z, Luck DJ (1982) Suppressor mutations in Chlamydomonas reveal a regulatory mechanism for Flagellar function. Cell 28:115-124

Rupp G, Porter ME (2003) A subunit of the dynein regulatory complex in Chlamydomonas is a homologue of a growth arrest-specific gene product. J Cell Biol 162:47-57


  • Locus:
  • SUP-PF3 [PF2]
  • Chromosome:
  • 11

From Culture Centre of Algae and Protozoa (CCAP), December 1982

Phenotype: impaired motility

Please see CC-1031 for more information on the PF12 locus.


  • Locus:
  • PF12
  • Chromosome:
  • 2

From Culture Centre of Algae and Protozoa (CCAP), December 1982

Phenotype: impaired motility

Please see CC-1030 for more information on the PF13 locus.


  • Locus:
  • PF13
  • Chromosome:
  • 9