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  • The Company of Biologists  (3)
  • English  (3)
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  • The Company of Biologists  (3)
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  • English  (3)
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  • 1
    In: Development, The Company of Biologists, Vol. 114, No. 2 ( 1992-02-01), p. 317-330
    Abstract: The pattern of autofluorescence in the two free-living soil nematodes Rhabditis dolichura and Caenorhabditis elegans has been compared. In C. elegans, during later embryogenesis the prospective gut cells develop a typical bluish autofluorescence as seen under UV illumination, while in Rh. dolichura a strong autofluorescence is already present in the unfertilized egg. Using a new, lowcost signal enhancement device, we have been able to follow in vivo the dramatic change in the pattern of autofluorescence during embryogenesis of Rh. dolichura. Autofluorescent material accumulates progressively in the gut primordium and disappears completely from all other cells. To investigate whether such an accumulation of cytoplasmic components also takes place in the C. elegans embryo, we labeled the cytoplasm of the egg with the fluorescing tracer dyes Lucifer Yellow (LY) or Rhodamine 6G (R6G). While LY appears to bind to yolk and progressively accumulates in the developing gut primordium, R6G does not show any such binding and remains equally distributed over all cells. Measurements in early and late stages indicate a significant increase in the volume of the gut cells during embryogenesis, while the embryo as a whole does not grow. Moreover, in cleavage-blocked 2-cell stages after development overnight, a reversal of cell size relationship to the benefit of the gut precursor cell takes place. In summary, our observations suggest a previously unknown massive transfer of yolk components in the nematode embryo from non-gut cells into lysosomes of the gut primordium, where they are further metabolized during postembryonic development.
    Type of Medium: Online Resource
    ISSN: 0950-1991 , 1477-9129
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 1992
    detail.hit.zdb_id: 2007916-3
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    The Company of Biologists ; 1986
    In:  Development Vol. 97, No. Supplement ( 1986-10-01), p. 31-44
    In: Development, The Company of Biologists, Vol. 97, No. Supplement ( 1986-10-01), p. 31-44
    Type of Medium: Online Resource
    ISSN: 0950-1991 , 1477-9129
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 1986
    detail.hit.zdb_id: 2007916-3
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    The Company of Biologists ; 1995
    In:  Development Vol. 121, No. 9 ( 1995-09-01), p. 2961-2972
    In: Development, The Company of Biologists, Vol. 121, No. 9 ( 1995-09-01), p. 2961-2972
    Abstract: Mutations in the maternal-effect sterile gene mes-1 cause the offspring of homozygous mutant mothers to develop into sterile adults. Lineage analysis revealed that mutant offspring are sterile because they fail to form primordial germ cells during embryogenesis. In wild-type embryos, the primordial germ cell P4 is generated via a series of four unequal stem-cell divisions of the zygote. mes-1 embryos display a premature and progressive loss of polarity in these divisions: P0 and P1 undergo apparently normal unequal divisions and cytoplasmic partitioning, but P2 (in some embryos) and P3 (in most embryos) display defects in cleavage asymmetry and fail to partition lineage-specific components to only one daughter cell. As an apparent con-sequence of these defects, P4 is transformed into a muscle precursor, like its somatic sister cell D, and generates up to 20 body muscle cells instead of germ cells. Our results show that the wild-type mes-1 gene participates in promoting unequal germ-line divisions and asymmetric partitioning events and thus the determination of cell fate in early C. elegans embryos.
    Type of Medium: Online Resource
    ISSN: 0950-1991 , 1477-9129
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 1995
    detail.hit.zdb_id: 2007916-3
    SSG: 12
    Location Call Number Limitation Availability
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