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Baker BS, Carpenter AT, Ripoll P. The Utilization during Mitotic Cell Division of Loci Controlling Meiotic Recombination and Disjunction in DROSOPHILA MELANOGASTER. Genetics. 1978;90(3):531-78doi: 10.1093/genetics/90.3.531.
Baker, B. S., Carpenter, A. T., & Ripoll, P. (1978). The Utilization during Mitotic Cell Division of Loci Controlling Meiotic Recombination and Disjunction in DROSOPHILA MELANOGASTER. Genetics, 90(3), 531-78. https://doi.org/10.1093/genetics/90.3.531
Baker, B S, et al. "The Utilization during Mitotic Cell Division of Loci Controlling Meiotic Recombination and Disjunction in DROSOPHILA MELANOGASTER." Genetics vol. 90,3 (1978): 531-78. doi: https://doi.org/10.1093/genetics/90.3.531
Baker BS, Carpenter AT, Ripoll P. The Utilization during Mitotic Cell Division of Loci Controlling Meiotic Recombination and Disjunction in DROSOPHILA MELANOGASTER. Genetics. 1978 Nov;90(3):531-78. doi: 10.1093/genetics/90.3.531. PMID: 17248870; PMCID: PMC1213905.
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Genetics. 1978 Nov;90(3):531-78. doi: 10.1093/genetics/90.3.531.

The Utilization during Mitotic Cell Division of Loci Controlling Meiotic Recombination and Disjunction in DROSOPHILA MELANOGASTER.

Genetics

B S Baker, A T Carpenter, P Ripoll

Affiliations

  1. Department of Biology, University of California, San Diego, La Jolla, California 92093.

PMID: 17248870 PMCID: PMC1213905 DOI: 10.1093/genetics/90.3.531

Abstract

To inquire whether the loci identified by recombination-defective and disjunction-defective meiotic mutants in Drosophila are also utilized during mitotic cell division, the effects of 18 meiotic mutants (representing 13 loci) on mitotic chromosome stability have been examined genetically. To do this, meiotic-mutant-bearing flies heterozygous for recessive somatic cell markers were examined for the frequencies and types of spontaneous clones expressing the cell markers. In such flies, marked clones can arise via mitotic recombination, mutation, chromosome breakage, nondisjunction or chromosome loss, and clones from these different origins can be distinguished. In addition, meiotic mutants at nine loci have been examined for their effects on sensitivity to killing by UV and X rays.-Mutants at six of the seven recombination-defective loci examined (mei-9, mei-41, c(3)G, mei-W68, mei-S282, mei-352, mei-218) cause mitotic chromosome instability in both sexes, whereas mutants at one locus (mei-218) do not affect mitotic chromosome stability. Thus many of the loci utilized during meiotic recombination also function in the chromosomal economy of mitotic cells.-The chromosome instability produced by mei-41 alleles is the consequence of chromosome breakage, that of mei-9 alleles is primarily due to chromosome breakage and, to a lesser extent, to an elevated frequency of mitotic recombination, whereas no predominant mechanism responsible for the instability caused by c(3)G alleles is discernible. Since these three loci are defective in their responses to mutagen damage, their effects on chromosome stability in nonmutagenized cells are interpreted as resulting from an inability to repair spontaneous lesions. Both mei-W68 and mei-S282 increase mitotic recombination (and in mei-W68, to a lesser extent, chromosome loss) in the abdomen but not the wing. In the abdomen, the primary effect on chromosome stability occurs during the larval period when the abdominal histoblasts are in a nondividing (G2) state.-Mitotic recombination is at or above control levels in the presence of each of the recombination-defective meiotic mutants examined, suggesting that meiotic and mitotic recombination are under separate genetic control in Drosophila.-Of the six mutants examined that are defective in processes required for regular meiotic chromosome segregation, four (l(1)TW-6(cs), ca(nd), mei-S332, ord) affect mitotic chromosome behavior. At semi-restrictive temperatures, the cold sensitive lethal l(1)TW-6(cs) causes very frequent somatic spots, a substantial proportion of which are attributable to nondisjunction or loss. Thus, this locus specifies a function essential for chromosome segregation at mitosis as well as at the first meiotic division in females. The patterns of mitotic effects caused by ca(nd), mei-S332, and ord suggest that they may be leaky alleles at essential loci that specify functions common to meiosis and mitosis. Mutants at the two remaining loci (nod, pal) do not affect mitotic chromosome stability.

References

  1. Genetics. 1929 Jul;14(4):366-419 - PubMed
  2. Mol Gen Genet. 1975;136(1):75-86 - PubMed
  3. Genetics. 1969 Mar;61(3):577-94 - PubMed
  4. Science. 1946 May 3;103(2679):553-4 - PubMed
  5. Philos Trans R Soc Lond B Biol Sci. 1977 Mar 21;277(955):295-312 - PubMed
  6. Genetics. 1976 Nov;84(3):485-506 - PubMed
  7. Nature. 1976 Dec 23-30;264(5588):719-22 - PubMed
  8. Genetics. 1975 Apr;79(4):589-99 - PubMed
  9. Genetics. 1975 Jun;80(2):267-96 - PubMed
  10. Genetics. 1976 Nov;84(3):507-26 - PubMed
  11. Genetics. 1976 Nov;84(3):527-44 - PubMed
  12. Proc Natl Acad Sci U S A. 1974 Nov;71(11):4508-12 - PubMed
  13. Annu Rev Genet. 1973;7:67-86 - PubMed
  14. Dev Biol. 1973 Jun;32(2):361-72 - PubMed
  15. Genetics. 1974 Mar;76(3):453-75 - PubMed
  16. Genet Res. 1974 Feb;23(1):1-12 - PubMed
  17. Genetics. 1974 Sep;78(1):289-97 - PubMed
  18. Aust J Biol Sci. 1974 Apr;27(2):219-29 - PubMed
  19. Mol Gen Genet. 1973 Sep 12;125(3):197-216 - PubMed
  20. Genetics. 1974 Aug;77(4):687-700 - PubMed
  21. Ann Genet. 1972 Mar;15(1):29-40 - PubMed
  22. Mol Gen Genet. 1972;115(1):54-72 - PubMed
  23. Genetics. 1972 May;71(1):157-84 - PubMed
  24. Genetics. 1972 Jul;71(3):367-400 - PubMed
  25. Genetics. 1973 Mar;73(3):393-428 - PubMed
  26. Dev Biol. 1971 Jan;24(1):61-87 - PubMed
  27. Mol Gen Genet. 1971;113(3):251-72 - PubMed
  28. Dev Biol. 1970 Jul;22(3):389-411 - PubMed
  29. Mol Gen Genet. 1970;107(4):291-304 - PubMed
  30. Genetics. 1968 Nov;60(3):525-58 - PubMed
  31. Humangenetik. 1964;1(2):194-6 - PubMed
  32. Genetics. 1966 Jan;53(1):157-64 - PubMed
  33. Genetics. 1953 Nov;38(6):630-51 - PubMed

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