Strains

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD76.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

  • Locus:
  • ARS5
  • Chromosome:
  • 10

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

  • Locus:
  • ARS5
  • Chromosome:
  • 10

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

  • Locus:
  • ARS5
  • Chromosome:
  • 10

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

  • Locus:
  • ARS5
  • Chromosome:
  • 10

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

  • Locus:
  • ARS5
  • Chromosome:
  • 10

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

  • Locus:
  • ARS5
  • Chromosome:
  • 10

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

  • Locus:
  • ARS5
  • Chromosome:
  • 10

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

  • Locus:
  • ARS5
  • Chromosome:
  • 10

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

  • Locus:
  • ARS5
  • Chromosome:
  • 10

From John Davies, Iowa State University, August 2000

Phenotype: altered sulfur metabolism

Derived by transformation of CC-425 with pJD67.

This strain has low arylsulfatase activity when grow under sulfur-deficient conditions.

  • Locus:
  • ARS5
  • Chromosome:
  • 10

From David Polley, Wabash College, September 2000

Phenotype: requires high potassium concentration

This mutant requires potassium concentrations greater than 0.1mM for growth. Use agarose solidified medium when testing for phenotype on plate cultures. Wild-type growth rates require 1mM K. Exhibits altered transport kinetics.
This mutant was UV-induced by Polley and Doctor in a strain equivalent to CC-620 (137c background).

Polley LD, Doctor DD (1985) Potassium transport in Chlamydomonas reinhardtii: isolation and characterization of transport-deficient mutant strains. Planta 163:208-213

Polley LD (1999) Genetic analysis of mutant clones of Chlamydomonas reinhardtii defective in potassium transport. Mol Gen Genet 261:275-280

  • Locus:
  • TRK3
  • Chromosome:
  • 3

From David Polley, Wabash College, September 2000

Phenotype: requires high potassium concentration

This mutant requires potassium concentrations greater than 0.1mM for growth. Use agarose solidified medium when testing for phenotype on plate cultures. Wild-type growth rates require 1mM K. Exhibits altered transport kinetics.
This mutant was UV-induced by Polley in CC-125.

Polley LD (1999) Genetic analysis of mutant clones of Chlamydomonas reinhardtii defective in potassium transport. Mol Gen Genet 261:275-280

  • Locus:
  • TRK2
  • Chromosome:
  • 2

From Malcolm Campbell, Davidson College, September 2000

Phenotype: does not mate

This mutant was obtained in a screen for mutants impaired in mating or zygote formation, and was characterized as being unable to agglutinate with gametes of either mating type. This is an insertional mutation made by transformation with the ARG7 gene. The affected gene was identified as the PMH1 gene, which encodes a plasma membrane hydrogen ATPase.

Campbell AM, Coble AJ, Cohen LD, Ch'Ng TH, Russo KM, Long EM, Armbrust EV (2001) Identification and DNA sequence of a new H+-ATPase in the unicellular green alga Chlamydomonas reinhardtii (CHLOROPHYCEAE). J. Phycol 37:536-642

  • Locus:
  • PMH1 [ACA3]
  • Chromosome:
  • 3

From Malcolm Campbell, Davidson College, September 2000

Phenotype: does not mate

This is the iso1 mutation in a mt+ background, Campbell strain “G2 iso+.” Please see CC-2926 for more information on iso1.

From Malcolm Campbell, Davidson College, September 2000

Phenotype: does not mate; requires acetate

This is the iso1 ARG7 insertion mutation coupled with the ac17 mutation, and was received as Campbell strain G1.48. Please see CC-2926 for more information on iso1.

  • Locus:
  • AC17
  • Chromosome:
  • 3

From Malcolm Campbell, Davidson College, September 2000

Phenotype: does not mate

This is an iso1 mutation obtained by NIT1 insertion in a mt- background, and was received as Campbell strain MB1 G1.48 NIT+. Please see CC-2926 for more information on the phenotype of iso1.

From Malcolm Campbell, Davidson College, September 2000

Phenotype: does not mate

This was received as Campbell’s “H5 dip” and is a mt+/mt- diploid strain whose parental strains were CC-3834 and CC-2926.

From Malcolm Campbell, Davidson College, September 2000

This is an iso1 ARG insertional mutant whose phenotype is suppressed. Similar suppression is observed in iso1 strains that are not transferred frequently. Campbell was unable to remove the suppression by outcrossing.

From Malcolm Campbell, Davidson College, September 2000

Phenotype: does not mate

This is presumed to be identical to CC-2926.

From Masa Kitayama, Ehime Women’s College, October 2000

Phenotype: requires acetate; chlorophyll deficient; antibiotic resistant (spectinomycin, streptomycin)

This mutant was originally obtained by Jon Suzuki, by co-transformation of strain 2137 (see CC-3269) with P-183 carrying the spr-u-1-6-2 and sr-u-2-60 antibiotic resistance mutations, and a kanamycin/bleomycin resistance cassette that inserted into the chlL gene in the chloroplast genome.

Suzuki JY, Bauer CE (1992) Light-independent chlorophyll biosynthesis: involvement of the chloroplast gene chlL (frxC). Plant Cell 4:929-940

  • Locus:
  • chlL
  • Chromosome:
  • chloroplast

From Joel Rosenbaum, Yale University, January 2001

Phenotype: does not show gliding motility

The gli mutants were generated by Keith Kozminski using insertional mutagenesis, and are described in his Ph.D. thesis. The background strain was Kozminski’s KK30A3, a product from a cross between CC-1024 pf1 nit1 nit2 mt+ and KK25E5 nit1-305 mt- (which in turn was derived from a cross of a nit1305 mt+ strain to CC-2453 nit1305 mt-). Non-gliding mutants were selected by their compact colony morphology as described by Lewin (Experientia 38, 348-349, 1982).

The mutants were characterized by ability to adhere to a coverslip, to bind polystyrene beads to the flagellar membrane, and to translocate beads along the length of the flagellum.

Class I mutants are capable of all three of these activities.
Class II mutants adhere to coverslips but do not bind or translocate beads.
Class III mutants bind and translocate beads but do not adhere to coverslips.
Class IV mutants are deficient in all three activities.
Class V mutants adhere to coverslips, but only by their flagellar tips. They also bind and translocate beads.

Kozminksi concluded that different glycoproteins are probably involved in coverslip adhesion vs. binding beads (shown by classes II and III, and speculated that the Class IV mutants my be deficient in the previously characterized 350 kD protein of the flagellar membrane. He postulated that the Class I and Class V mutants could have alterations in regulation of gliding or in the gliding motor.

This mutant (T1B3) is in Class I.