Article thumbnail

Stress-Induced Loss of Heterozygosity in Candida: a Possible Missing Link in the Ability to Evolve

By Susan M. Rosenberg


Diploid organisms are buffered against the effects of mutations by carrying two sets of each gene, which allows compensation if one is mutated. But recombination between “mom” and “dad” chromosomes causes loss of heterozygosity (LOH), stretches of “mom-only” or “dad-only” DNA sequence, suddenly revealing effects of mutations accumulated in entire chromosome arms. LOH creates new phenotypes from old mutations, drives cancer development and evolution, and, in a new study by Forche et al., is shown to be induced by stress in Candida albicans [Forche A, et al, mBio 2(4):e00129-11, 2011]. Stress-induced LOH could speed evolution of Candida specifically when it is poorly adapted to its environment. Moreover, the findings may provide a missing link between recombination-dependent mutagenesis in bacteria and yeast, suggesting that both might be stress induced, both maximizing genetic variation when populations could benefit most from diversity

Topics: Commentary
Publisher: American Society of Microbiology
OAI identifier:
Provided by: PubMed Central

To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.

Suggested articles


  1. (1997). A role for REV3 in mutagenesis during double-strand break repair in Saccharomyces cerevisiae.
  2. (2005). A switch from highfidelity to error-prone DNA double-strand break repair underlies stressinduced mutation.
  3. (1994). Adaptive mutation by deletions in small mononucleotide repeats.
  4. (2008). Break-induced replication: what is it and what is it for? Cell Cycle 7:859–864.
  5. (1980). Control of recA gene RNA in E. coli: regulatory and signal genes.
  6. (2011). Damage-induced localized hypermutability.
  7. (1995). DNA synthesis errors associated with double-strand-break repair.
  8. (2010). Dr Jeckyll and Mr Hyde: role of aneuploidy in cellular adaptation and cancer.
  9. (1983). Expression of recessive alleles by chromosomal mechanisms in retinoblastoma.
  10. (2008). Hypermutability of damaged single-strand DNA formed at double-strand breaks and uncapped telomeres in yeast Saccharomyces cerevisiae. PLoS Genet.
  11. (2011). Impactofastress-inducibleswitchtomutagenicrepairofDNAbreakson mutation in Escherichia coli.
  12. (2010). Increased mutagenesis and unique mutation signature associated with mitotic gene conversion.
  13. (1978). Mechanisms that rapidly reorganize the genome. Stadler Symp.
  14. (1971). Mutation and cancer: statistical study of retinoblastoma.
  15. (2007). Mutation as a stress responseandtheregulationofevolvability.Crit.Rev.Biochem.Mol.Biol.
  16. (2010). Protein homeostasis and the phenotypic manifestation of genetic diversity: principles and mechanisms.
  17. RadmanM.1975.SOSrepairhypothesis:phenomenologyofaninducible DNA repair which is accompanied by mutagenesis. Basic Life Sci.
  18. (1994). Recombination in adaptive mutation.
  19. (2010). Separate DNA Pol II- and Pol IV-dependent pathways of stress-induced mutation during double-strand-break repair in Escherichia coli are controlled by RpoS.
  20. (2011). Stress alters rates and types of loss of heterozygosity in Candida albicans.
  21. (2009). Stressinduced beta-lactam antibiotic resistance mutation and sequences of stationary-phase mutations in the Escherichia coli chromosome.
  22. (1982). The growth of biological thought, diversity, evolution, and inheritance.