scholarly journals Cilia and the cell cycle?

2005 ◽  
Vol 169 (5) ◽  
pp. 707-710 ◽  
Author(s):  
Lynne M. Quarmby ◽  
Jeremy D.K. Parker
Keyword(s):  
Cell Cycle ◽  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Mammalian Cells ◽  
Cell Cycle Regulation ◽  
Polycystic Kidney ◽  
Unicellular Alga ◽  
Regulatory Relationship ◽  
Cycle Regulation ◽  
Multiple Signaling

A recent convergence of data indicating a relationship between cilia and proliferative diseases, such as polycystic kidney disease, has revived the long-standing enigma of the reciprocal regulatory relationship between cilia and the cell cycle. Multiple signaling pathways are localized to cilia in mammalian cells, and some proteins have been shown to act both in the cilium and in cell cycle regulation. Work from the unicellular alga Chlamydomonas is providing novel insights as to how cilia and the cell cycle are coordinately regulated.

Calcium and cell cycle control

Development ◽  
1990 ◽  
Vol 108 (4) ◽  
pp. 525-542 ◽  
Author(s):  
M. Whitaker ◽  
R. Patel
Keyword(s):  
Cell Cycle ◽  
Sea Urchin ◽  
Mammalian Cells ◽  
Cell Cycle Regulation ◽  
Sea Urchins ◽  
Cell Cycle Control ◽  
Control Point ◽  
Control Cell ◽  
Free Calcium ◽  
Cycle Regulation

The cell division cycle of the early sea urchin embryo is basic. Nonetheless, it has control points in common with the yeast and mammalian cell cycles, at START, mitosis ENTRY and mitosis EXIT. Progression through each control point in sea urchins is triggered by transient increases in intracellular free calcium. The Cai transients control cell cycle progression by translational and post-translational regulation of the cell cycle control proteins pp34 and cyclin. The START Cai transient leads to phosphorylation of pp34 and cyclin synthesis. The mitosis ENTRY Cai transient triggers cyclin phosphorylation. The motosis EXIT transient causes destruction of phosphorylated cyclin. We compare cell cycle regulation by calcium in sea urchin embryos to cell cycle regulation in other eggs and oocytes and in mammalian cells.

scholarly journals MicroRNA15a modulates expression of the cell-cycle regulator Cdc25A and affects hepatic cystogenesis in a rat model of polycystic kidney disease

2008 ◽  
Vol 118 (11) ◽  
pp. 3714-3724 ◽  
Author(s):  
Seung-Ok Lee ◽  
Tatyana Masyuk ◽  
Patrick Splinter ◽  
Jesús M. Banales ◽  
Anatoliy Masyuk ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Rat Model ◽  
Polycystic Kidney ◽  
Cell Cycle Regulator

scholarly journals Loss of polycystins suppresses deciliation via the activation of the centrosomal integrity pathway

2020 ◽  
Vol 3 (9) ◽  
pp. e202000750 ◽  
Author(s):  
Vasileios Gerakopoulos ◽  
Peter Ngo ◽  
Leonidas Tsiokas
Keyword(s):  
Cell Cycle ◽  
Kidney Disease ◽  
Signaling Pathways ◽  
Polycystic Kidney Disease ◽  
Primary Cilia ◽  
Autosomal Dominant ◽  
Polycystic Kidney ◽  
Cyclic Pattern ◽  
Autosomal Dominant Polycystic Kidney ◽  
Cystic Growth

The primary cilium is a microtubule-based, antenna-like organelle housing several signaling pathways. It follows a cyclic pattern of assembly and deciliation (disassembly and/or shedding), as cells exit and re-enter the cell cycle, respectively. In general, primary cilia loss leads to kidney cystogenesis. However, in animal models of autosomal dominant polycystic kidney disease, a major disease caused by mutations in the polycystin genes (Pkd1 or Pkd2), primary cilia ablation or acceleration of deciliation suppresses cystic growth, whereas deceleration of deciliation enhances cystogenesis. Here, we show that deciliation is delayed in the cystic epithelium of a mouse model of postnatal deletion of Pkd1 and in Pkd1- or Pkd2-null cells in culture. Mechanistic experiments show that PKD1 depletion activates the centrosomal integrity/mitotic surveillance pathway involving 53BP1, USP28, and p53 leading to a delay in deciliation. Reduced deciliation rate causes prolonged activation of cilia-based signaling pathways that could promote cystic growth. Our study links polycystins to cilia dynamics, identifies cellular deciliation downstream of the centrosomal integrity pathway, and helps explain pro-cystic effects of primary cilia in autosomal dominant polycystic kidney disease.

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