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Related Experiment Videos

Complementation of a red-light-indifferent cyanobacterial mutant.

G G Chiang1, M R Schaefer, A R Grossman

  • 1Department of Plant Biology, Carnegie Institution of Washington, Stanford, CA 94305.

Proceedings of the National Academy of Sciences of the United States of America
|October 15, 1992
PubMed
Summary

Mutant cyanobacteria strains FdR1 and FdR2 fail to adapt to red light due to insertions in the rcaC gene. This gene is crucial for complementary chromatic adaptation, regulating phycobilisome changes in response to light.

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Introduction.

Photosynthesis research·2005

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Cyanobacteria exhibit complementary chromatic adaptation (CCA), altering phycobilisome composition in response to light wavelength.
  • Mutant strains FdR1 and FdR2 of Fremyella diplosiphon display defective CCA, consistently responding as if under green light.

Purpose of the Study:

  • To identify the genetic basis of aberrant chromatic adaptation in FdR1 and FdR2 mutant strains.
  • To elucidate the role of the identified gene in the CCA signal transduction pathway.

Main Methods:

  • Complementation of mutant strains using a wild-type genomic library.
  • Genetic mapping and subcloning to localize the complementing DNA region.
  • Southern blot analysis to detect DNA insertions.

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  • Sequence analysis to predict protein function.

    • Main Results:

    • The complementing DNA was localized to a region containing the rcaC gene, which also complemented FdR2.
    • FdR1 and FdR2 strains possess DNA insertions within the rcaC gene, likely from transposable elements.
    • The RcaC protein sequence shows high similarity to bacterial response regulators.

    Conclusions:

    • The rcaC gene is essential for complementary chromatic adaptation in Fremyella diplosiphon.
    • RcaC likely functions as a response regulator in a two-component system mediating light-regulated gene expression.
    • Mutations in rcaC disrupt the signal transduction pathway controlling phycobilisome adjustments during CCA.