Lgl and its phosphorylation by aPKC regulate oocyte polarity formation in<i>Drosophila</i>

Tian, Aiqin; Deng, Wu-Min

doi:10.1242/dev.016253

Cited by 63 publications

(84 citation statements)

References 48 publications

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“…Recent studies have shown that Lgl is involved in the polarization of the A-P axis in the Drosophila oocyte (Doerflinger et al, 2010;Fichelson et al, 2010;Li et al, 2008;Tian and Deng, 2008). In the early oocyte, Lgl is required for the proper posterior translocation of cell fate determinants as well as the centrosomes (Fichelson et al, 2010;Tian and Deng, 2008).…”

Section: Introductionmentioning

confidence: 99%

TheC. eleganshomolog ofDrosophilaLethal giant larvae functions redundantly with PAR-2 to maintain polarity in the early embryo

2010

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SUMMARYPolarity is essential for generating cell diversity. The one-cell C. elegans embryo serves as a model for studying the establishment and maintenance of polarity. In the early embryo, a myosin II-dependent contraction of the cortical meshwork asymmetrically distributes the highly conserved PDZ proteins PAR-3 and PAR-6, as well as an atypical protein kinase C (PKC-3), to the anterior. The RING-finger protein PAR-2 becomes enriched on the posterior cortex and prevents these three proteins from returning to the posterior. In addition to the PAR proteins, other proteins are required for polarity in many metazoans. One example is the conserved Drosophila tumor-suppressor protein Lethal giant larvae (Lgl). In Drosophila and mammals, Lgl contributes to the maintenance of cell polarity and plays a role in asymmetric cell division. We have found that the C. elegans homolog of Lgl, LGL-1, has a role in polarity but is not essential. It localizes asymmetrically to the posterior of the early embryo in a PKC-3-dependent manner, and functions redundantly with PAR-2 to maintain polarity. Furthermore, overexpression of LGL-1 is sufficient to rescue loss of PAR-2 function.LGL-1 negatively regulates the accumulation of myosin (NMY-2) on the posterior cortex, representing a possible mechanism by which LGL-1 might contribute to polarity maintenance.

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Section: Introductionmentioning

confidence: 99%

TheC. eleganshomolog ofDrosophilaLethal giant larvae functions redundantly with PAR-2 to maintain polarity in the early embryo

2010

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“…10,18,19,[22][23][24][25][26] We and others have shown that lgl/dlg/scrib are required for a number of developmental controls during oogenesis. 10,[18][19][20]22,23,[27][28][29][30][31][32][33][34][35][36] In particular, we have identified Lgl as an essential regulator in PFC specification and differentiation, and a role of dlg/scrib in both anterior and posterior patterning of the follicular epithelium. 32,37 In this paper, we show that lgl genetically interacts with dlg/scrib in PFC fate induction, suggesting a common regulatory pathway in this process.…”

Section: Introductionmentioning

confidence: 99%

Requirements of Lgl in cell differentiation and motility during Drosophila ovarian follicular epithelium morphogenesis

Li¹,

Feng²,

Yu³

et al. 2011

Fly

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“…To examine the physiological function of aPKC in Hh signaling further, we used mitotic recombination to generate clones homozygous for aPKC K06403 , a strong allele of aPKC (35). We found that in aPKC mutant cells, Smo accumulated in apical membrane of wing disc ( Fig.…”

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confidence: 99%

Hedgehog-regulated atypical PKC promotes phosphorylation and activation of Smoothened and Cubitus interruptus in Drosophila

Jiang

Liu

Fan

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Significance Hedgehog (Hh) signaling by Smoothened (Smo) is mediated by phosphorylation and cell surface/cilium accumulation, but how the localization of Smo is controlled remains poorly understood. We show that the atypical PKC (aPKC)–partition defective 6 (Par6) complex promotes Hh signaling by phosphorylating Smo and regulating Smo basolateral accumulation in addition to phosphorylating the transcription factor cubitus interruptus (Ci). Our results demonstrate direct involvement of aPKC in Hh signaling beyond its role in cell polarity and suggest that basolateral accumulation of Smo is critical for its activity. Abnormal activation of Smo results in several types of cancers, and Smo can easily acquire drug resistance through mutations. A better understanding of the mechanisms of Smo regulation is critical to developing more effective therapeutic treatments for cancers caused by Smo dysregulation.

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Lgl and its phosphorylation by aPKC regulate oocyte polarity formation inDrosophila

Cited by 63 publications

References 48 publications

TheC. eleganshomolog ofDrosophilaLethal giant larvae functions redundantly with PAR-2 to maintain polarity in the early embryo

TheC. eleganshomolog ofDrosophilaLethal giant larvae functions redundantly with PAR-2 to maintain polarity in the early embryo

Requirements of Lgl in cell differentiation and motility during Drosophila ovarian follicular epithelium morphogenesis

Hedgehog-regulated atypical PKC promotes phosphorylation and activation of Smoothened and Cubitus interruptus in Drosophila

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