scholarly journals Katanin Knockdown Supports a Role for Microtubule Severing in Release of Basal Bodies before Mitosis in Chlamydomonas

2009 ◽  
Vol 20 (1) ◽  
pp. 379-388 ◽  
Author(s):  
M. Qasim Rasi ◽  
Jeremy D.K. Parker ◽  
Jessica L. Feldman ◽  
Wallace F. Marshall ◽  
Lynne M. Quarmby
Keyword(s):  
Cell Cycle ◽  
Rna Interference ◽  
Transition Zone ◽  
Basal Body ◽  
Cell Cycle Progression ◽  
Basal Bodies ◽  
Cycle Progression ◽  
Microtubule Severing ◽  
Regulation Of Cell Cycle ◽  
Precise Role

Katanin is a microtubule-severing protein that participates in the regulation of cell cycle progression and in ciliary disassembly, but its precise role is not known for either activity. Our data suggest that in Chlamydomonas, katanin severs doublet microtubules at the proximal end of the flagellar transition zone, allowing disengagement of the basal body from the flagellum before mitosis. Using an RNA interference approach we have discovered that severe knockdown of the p60 subunit of katanin, KAT1, is achieved only in cells that also carry secondary mutations that disrupt ciliogenesis. Importantly, we observed that cells in the process of cell cycle-induced flagellar resorption sever the flagella from the basal bodies before resorption is complete, and we find that this process is defective in KAT1 knockdown cells.

The FA2 gene of Chlamydomonas encodes a NIMA family kinase with roles in cell cycle progression and microtubule severing during deflagellation

2002 ◽  
Vol 115 (8) ◽  
pp. 1759-1768 ◽  
Author(s):  
Moe R. Mahjoub ◽  
Ben Montpetit ◽  
Lifan Zhao ◽  
Rip J. Finst ◽  
Benjamin Goh ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Chlamydomonas Reinhardtii ◽  
Basal Body ◽  
Cell Cycle Progression ◽  
Chromatin Condensation ◽  
Eukaryotic Cell ◽  
Genetic Screen ◽  
Cycle Progression ◽  
Microtubule Severing

The NIMA kinases are one of several families of kinases that participate in driving the eukaryotic cell cycle. NIMA-related kinases have been implicated in G2/M progression, chromatin condensation and regulation of the centrosome cycle. Here we report the identification of a new member of this family, FA2, from Chlamydomonas reinhardtii. FA2 was originally discovered in a genetic screen for deflagellation-defective mutants. We have previously shown that FA2 is essential for basal-body/centriole-associated microtubule severing. We now report that the FA2 NIMA-related kinase also plays a role in cell cycle progression in Chlamydomonas. This is the first indication that members of the NIMA family might exert their effects through the regulation of microtubule severing.

PTTG has a Dual Role of Promotion-Inhibition in the Development of Pituitary Adenomas

2019 ◽  
Vol 26 (11) ◽  
pp. 800-818
Author(s):  
Zujian Xiong ◽  
Xuejun Li ◽  
Qi Yang
Keyword(s):  
Cell Cycle ◽  
Pituitary Adenoma ◽  
Pituitary Adenomas ◽  
Cell Cycle Progression ◽  
Key Factors ◽  
Cycle Progression ◽  
Sister Chromatids ◽  
Regulation Of Cell Cycle ◽  
Late Stages

Pituitary Tumor Transforming Gene (PTTG) of human is known as a checkpoint gene in the middle and late stages of mitosis, and is also a proto-oncogene that promotes cell cycle progression. In the nucleus, PTTG works as securin in controlling the mid-term segregation of sister chromatids. Overexpression of PTTG, entering the nucleus with the help of PBF in pituitary adenomas, participates in the regulation of cell cycle, interferes with DNA repair, induces genetic instability, transactivates FGF-2 and VEGF and promotes angiogenesis and tumor invasion. Simultaneously, overexpression of PTTG induces tumor cell senescence through the DNA damage pathway, making pituitary adenoma possessing the potential self-limiting ability. To elucidate the mechanism of PTTG in the regulation of pituitary adenomas, we focus on both the positive and negative function of PTTG and find out key factors interacted with PTTG in pituitary adenomas. Furthermore, we discuss other possible mechanisms correlate with PTTG in pituitary adenoma initiation and development and the potential value of PTTG in clinical treatment.

scholarly journals Centrin Gene Disruption Impairs Stage-specific Basal Body Duplication and Cell Cycle Progression inLeishmania

2004 ◽  
Vol 279 (24) ◽  
pp. 25703-25710 ◽  
Author(s):  
Angamuthu Selvapandiyan ◽  
Alain Debrabant ◽  
Robert Duncan ◽  
Jacqueline Muller ◽  
Poonam Salotra ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Basal Body ◽  
Gene Disruption ◽  
Cell Cycle Progression ◽  
Cycle Progression

Estrogen Regulation of Cell Cycle Progression

2001 ◽  
pp. 220-227
Author(s):  
Owen W. J. Prall ◽  
Eileen M. Rogan ◽  
Elizabeth A. Musgrove ◽  
Colin K. W. Watts ◽  
Robert L. Sutherland
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Estrogen Regulation ◽  
Cycle Progression ◽  
Regulation Of Cell Cycle

scholarly journals Regulation of cell cycle drivers by Cullin-RING ubiquitin ligases

2020 ◽  
Vol 52 (10) ◽  
pp. 1637-1651 ◽  
Author(s):  
Sang-Min Jang ◽  
Christophe E. Redon ◽  
Bhushan L. Thakur ◽  
Meriam K. Bahta ◽  
Mirit I. Aladjem
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Cycle Progression ◽  
Ubiquitin Ligases ◽  
Anaphase Promoting Complex ◽  
Cycle Progression ◽  
Cellular Processes ◽  
Cellular Pathways ◽  
Regulation Of Cell Cycle ◽  
F Box Protein

Abstract The last decade has revealed new roles for Cullin-RING ubiquitin ligases (CRLs) in a myriad of cellular processes, including cell cycle progression. In addition to CRL1, also named SCF (SKP1-Cullin 1-F box protein), which has been known for decades as an important factor in the regulation of the cell cycle, it is now evident that all eight CRL family members are involved in the intricate cellular pathways driving cell cycle progression. In this review, we summarize the structure of CRLs and their functions in driving the cell cycle. We focus on how CRLs target key proteins for degradation or otherwise alter their functions to control the progression over the various cell cycle phases leading to cell division. We also summarize how CRLs and the anaphase-promoting complex/cyclosome (APC/C) ligase complex closely cooperate to govern efficient cell cycle progression.

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