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  • 1985-1989  (2)
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  • 1
    ISSN: 1432-0983
    Keywords: Chlamydomonas monoica ; DAPI ; Mating type ; Uniparental inheritance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The Chlamydomonas monoica mutant allele mtl-1, is associated with the formation of nonviable zygospores following “self-mating” of the mutant strain. Furthermore, mtl-1 heterozygote populations show a 50% reduction in germination frequency and no transmission of a chloroplast antibiotic resistance marker carried by the mtl-1 parent. To determine whether the effects on zygospore viability and chloroplast gene transmission resulted from the direct involvement of the mtl-1 locus in the control of mt +-directed uniparental inheritance of chloroplast DNA (cpDNA), we have used the DNA-specific fluorochrome DAPI to follow the fate of cpDNA during the maturation of zygotes. Throughout the first few hours after the initial fusion of gametes, the young zygotes show DAPI-fluorescent nucleoids distributed symmetrically around the region of nuclear fusion, and presumably located within both of the parental chloroplasts. Wild-type and mtl-1 mutant zygotes show similar early staining patterns. As the zygotes age, the staining patterns become asymmetric for the wildtype population, with all of the visible cytoplasmic nucleoids restricted to one “side” of the zygote. In contrast, mtl-1 homozygotes appear to lose cytoplasmic nucleoids from both “sides” of the zygote simultaneously and within 24 h are apparently devoid of cpDNA. By introducing a mutation which arrests cell fusion (and prevents plastid fusion), we can show that (1) the asymmetric nucleoid distribution in wildtype zygotes results from the loss of nucleoids from one gamete in each mating event, and (2) the additional loss of cpDNA in mtl-1 homozygotes does not require contact between parental plastids (thus the nuclease responsible for cpDNA degradation is not sequestered within the chloroplast of one gamete). We propose that the mtl-1 mutant strain is defective for a process which normally protects cpDNA of mt + origin.
    Type of Medium: Electronic Resource
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  • 2
    Publication Date: 1988-04-01
    Print ISSN: 0172-8083
    Electronic ISSN: 1432-0983
    Topics: Biology
    Published by Springer
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