scholarly journals Planar cell polarity effector gene Intu regulates cell fate-specific differentiation of keratinocytes through the primary cilia

2012 ◽  
Vol 20 (1) ◽  
pp. 130-138 ◽  
Author(s):  
D Dai ◽  
L Li ◽  
A Huebner ◽  
H Zeng ◽  
E Guevara ◽  
...  
Keyword(s):  
Cell Fate ◽  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Primary Cilia ◽  
Effector Gene ◽  
Specific Differentiation

scholarly journals Loss of Planar Cell Polarity Effector Fuzzy Causes Renal Hypoplasia by Disrupting Several Signaling Pathways

2021 ◽  
Vol 10 (1) ◽  
pp. 1
Author(s):  
Irene-Yanran Wang ◽  
Chen-Fang Chung ◽  
Sima Babayeva ◽  
Tamara Sogomonian ◽  
Elena Torban
Keyword(s):  
Signaling Pathways ◽  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Primary Cilia ◽  
Branching Morphogenesis ◽  
Effector Proteins ◽  
Renal Hypoplasia ◽  
Developmental Disturbance ◽  
Pathways Analysis ◽  
Nephron Progenitor

In vertebrates, the planar cell polarity (PCP) pathway regulates tissue morphogenesis during organogenesis, including the kidney. Mutations in human PCP effector proteins have been associated with severe syndromic ciliopathies. Importantly, renal hypoplasia has been reported in some patients. However, the developmental disturbance that causes renal hypoplasia is unknown. Here, we describe the early onset of profound renal hypoplasia in mice homozygous for null mutation of the PCP effector gene, Fuzzy. We found that this phenotype is caused by defective branching morphogenesis of the ureteric bud (UB) in the absence of defects in nephron progenitor specification or in early steps of nephrogenesis. By using various experimental approaches, we show that the loss of Fuzzy affects multiple signaling pathways. Specifically, we found mild involvement of GDNF/c-Ret pathway that drives UB branching. We noted the deficient expression of molecules belonging to the Bmp, Fgf and Shh pathways. Analysis of the primary cilia in the UB structures revealed a significant decrease in ciliary length. We conclude that renal hypoplasia in the mouse Fuzzy mutants is caused by defective UB branching associated with dysregulation of ciliary and non-ciliary signaling pathways. Our work suggests a PCP effector-dependent pathogenetic mechanism that contributes to renal hypoplasia in mice and humans.

scholarly journals PLK-1 Regulation of Asymmetric Cell Division in the Early C. elegans Embryo

2021 ◽  
Vol 8 ◽  
Author(s):  
Amelia J. Kim ◽  
Erik E. Griffin
Keyword(s):  
Cell Division ◽  
Cell Fate ◽  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Asymmetric Cell Division ◽  
Critical Role ◽  
Cell Cortex ◽  
C Elegans ◽  
Mitotic Kinase ◽  
Centrosome Separation

PLK1 is a conserved mitotic kinase that is essential for the entry into and progression through mitosis. In addition to its canonical mitotic functions, recent studies have characterized a critical role for PLK-1 in regulating the polarization and asymmetric division of the one-cell C. elegans embryo. Prior to cell division, PLK-1 regulates both the polarization of the PAR proteins at the cell cortex and the segregation of cell fate determinants in the cytoplasm. Following cell division, PLK-1 is preferentially inherited to one daughter cell where it acts to regulate the timing of centrosome separation and cell division. PLK1 also regulates cell polarity in asymmetrically dividing Drosophila neuroblasts and during mammalian planar cell polarity, suggesting it may act broadly to connect cell polarity and cell cycle mechanisms.

scholarly journals Aberrant planar cell polarity induced by urinary tract obstruction

2009 ◽  
Vol 297 (6) ◽  
pp. F1526-F1533 ◽  
Author(s):  
Ling Li ◽  
Diana Zepeda-Orozco ◽  
Vishal Patel ◽  
Phu Truong ◽  
Courtney M. Karner ◽  
...  
Keyword(s):  
Cell Division ◽  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Primary Cilia ◽  
Urinary Tract Obstruction ◽  
Obstructive Uropathy ◽  
Mechanical Strain ◽  
Urine Flow ◽  
Tubular Diameter ◽  
Tubular Dilatation

Flow sensing by primary cilia of the epithelial cells is involved in cystogenesis in polycystic kidney disease. We investigate whether a similar mechanism applies to the pathogenesis of cyst-like tubular dilatation induced by ureteral obstruction in mice. Robust proliferation occurs in the obstructed tubules when urine flow is interrupted as well as in the repairing tubules when urine flow is reestablished after relief of the obstruction, suggesting a urine flow-independent mechanism of proliferation. In the urothelium, proliferation is only detected above the obstruction, although urine flow ceased both above and below the obstruction. Our results support mechanical strain- rather than flow-mediated proliferation in obstructive uropathy. To understand the mechanism of cell proliferation leading to increased tubular diameter in cyst-like tubular dilatation, we examine planar cell polarity (PCP), which is necessary for oriented cell division and maintenance of tubular diameter. In dilated tubules, the orientation of cell division is randomized, atypical PKC (aPKC) is mislocalized, and the pattern of the expression of a core PCP protein, Frizzled3 (Fz3), is altered. In addition, the level of Fz3 expression is increased. These results indicate that aberrant PCP may contribute to cyst-like tubular dilatation in obstructive uropathy. Interestingly, the orientation of cell division, localization of aPKC, and Fz3 expression return to normal when obstruction is relieved, which suggest a role of normal PCP signaling in tubular repair.

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