par-6, a gene involved in the establishment of asymmetry in early C. elegans embryos, mediates the asymmetric localization of PAR-3

Jennifer L. Watts, Bijan Etemad-Moghadam, Su Guo, Lynn Boyd, Bruce W. Draper, Craig C. Mello, James R. Priess, Kenneth J. Kemphues

Research output: Contribution to journalArticle

201 Citations (Scopus)

Abstract

The generation of asymmetry in the one-cell embryo of Caenorhabditis elegans is necessary to establish the anterior-posterior axis and to ensure the proper identity of early blastomeres. Maternal-effect lethal mutations with a partitioning defective phenotype (par) have identified several genes involved in this process. We have identified a new gene, par-6, which acts in conjunction with other par genes to properly localize cytoplasmic components in the early embryo. The early phenotypes of par-6 embryos include the generation of equal-sized blastomeres, improper localization of P granules and SKN-1 protein, and abnormal second division cleavage patterns. Overall, this phenotype is very similar to that caused by mutations in a previously described gene, par-3. The probable basis for this similarity is revealed by our genetic and immunolocalization results; par-6 acts through par-3 by localizing or maintaining the PAR-3 protein at the cell periphery. In addition, we find that loss-of-function par-6 mutations act as dominant bypass suppressors of loss-of-function mutations in par-2.

Original languageEnglish (US)
Pages (from-to)3133-3140
Number of pages8
JournalDevelopment
Volume122
Issue number10
StatePublished - 1996
Externally publishedYes

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Embryonic Structures
Blastomeres
Mutation
Phenotype
Genes
Caenorhabditis elegans
Proteins

Keywords

  • Assymmetry
  • Axis
  • Caenorhabditis elegans
  • Cell polarity
  • Embryogenesis
  • par-6
  • Suppression

ASJC Scopus subject areas

  • Anatomy
  • Cell Biology

Cite this

Watts, J. L., Etemad-Moghadam, B., Guo, S., Boyd, L., Draper, B. W., Mello, C. C., ... Kemphues, K. J. (1996). par-6, a gene involved in the establishment of asymmetry in early C. elegans embryos, mediates the asymmetric localization of PAR-3. Development, 122(10), 3133-3140.

par-6, a gene involved in the establishment of asymmetry in early C. elegans embryos, mediates the asymmetric localization of PAR-3. / Watts, Jennifer L.; Etemad-Moghadam, Bijan; Guo, Su; Boyd, Lynn; Draper, Bruce W.; Mello, Craig C.; Priess, James R.; Kemphues, Kenneth J.

In: Development, Vol. 122, No. 10, 1996, p. 3133-3140.

Research output: Contribution to journalArticle

Watts, JL, Etemad-Moghadam, B, Guo, S, Boyd, L, Draper, BW, Mello, CC, Priess, JR & Kemphues, KJ 1996, 'par-6, a gene involved in the establishment of asymmetry in early C. elegans embryos, mediates the asymmetric localization of PAR-3', Development, vol. 122, no. 10, pp. 3133-3140.
Watts JL, Etemad-Moghadam B, Guo S, Boyd L, Draper BW, Mello CC et al. par-6, a gene involved in the establishment of asymmetry in early C. elegans embryos, mediates the asymmetric localization of PAR-3. Development. 1996;122(10):3133-3140.
Watts, Jennifer L. ; Etemad-Moghadam, Bijan ; Guo, Su ; Boyd, Lynn ; Draper, Bruce W. ; Mello, Craig C. ; Priess, James R. ; Kemphues, Kenneth J. / par-6, a gene involved in the establishment of asymmetry in early C. elegans embryos, mediates the asymmetric localization of PAR-3. In: Development. 1996 ; Vol. 122, No. 10. pp. 3133-3140.
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AU - Boyd, Lynn

AU - Draper, Bruce W.

AU - Mello, Craig C.

AU - Priess, James R.

AU - Kemphues, Kenneth J.

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AB - The generation of asymmetry in the one-cell embryo of Caenorhabditis elegans is necessary to establish the anterior-posterior axis and to ensure the proper identity of early blastomeres. Maternal-effect lethal mutations with a partitioning defective phenotype (par) have identified several genes involved in this process. We have identified a new gene, par-6, which acts in conjunction with other par genes to properly localize cytoplasmic components in the early embryo. The early phenotypes of par-6 embryos include the generation of equal-sized blastomeres, improper localization of P granules and SKN-1 protein, and abnormal second division cleavage patterns. Overall, this phenotype is very similar to that caused by mutations in a previously described gene, par-3. The probable basis for this similarity is revealed by our genetic and immunolocalization results; par-6 acts through par-3 by localizing or maintaining the PAR-3 protein at the cell periphery. In addition, we find that loss-of-function par-6 mutations act as dominant bypass suppressors of loss-of-function mutations in par-2.

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