scholarly journals Heat Shock, Histone H3 Phosphorylation and the Cell Cycle

Cell Cycle ◽  
2004 ◽  
Vol 4 (1) ◽  
pp. 13-17 ◽  
Author(s):  
Mark H. Dyson ◽  
Stuart Thomson ◽  
Louis C. Mahadevan
2001 ◽  
Vol 12 (11) ◽  
pp. 3527-3537 ◽  
Author(s):  
Olga A. Cabello ◽  
Elena Eliseeva ◽  
WeiGong He ◽  
Hagop Youssoufian ◽  
Sharon E. Plon ◽  
...  

Condensin is a conserved 13S heteropentamer composed of two nonidentical structural maintenance of chromosome (SMC) family proteins, in Xenopus XCAP-C and XCAP-E, and three regulatory subunits, XCAP-D2, XCAP-G, and XCAP-H. Both biochemical and genetic analyses have demonstrated an essential role for the 13S condensin complex in mitotic chromosome condensation. Further, a potential requirement for condensin in completion of chromatid arm separation in early anaphase is demonstrated by the mutational phenotypes of the Drosophila homologues ofXCAP-H, barren and XCAP-C,DmSMC4. In this study we have investigated the expression and subcellular distribution of hCAP-H, the human homolog of XCAP-H, in order to better understand its cellular functions. Transcription of hCAP-H was restricted to proliferating cells with highest expression during the G2 phase of the cell cycle. In contrast, cellular hCAP-H protein levels were constant throughout the cell cycle. hCAP-H was found to be associated with mitotic chromosomes exhibiting a nonuniform but symmetric distribution along sister chromatids. The symmetry of hCAP-H association with sister chromatids suggests that there are sequence-dependent domains of condensin aggregation. During interphase hCAP-H, -C, and -E, have distinct punctate nucleolar localization, suggesting that condensin may associate with and modulate the conformation and function of rDNA. hCAP-H association with condensed chromatin was not observed in the early phase of chromosome condensation when histone H3 phosphorylation has already taken place. This finding is consistent with the hypothesis that histone H3 phosphorylation precedes condensin-mediated condensation.


2006 ◽  
Vol 20 (5) ◽  
Author(s):  
Rebecca Claire Chiffer ◽  
Sara K. Snyder ◽  
Pedro Rodriguez ◽  
Eric Anderson ◽  
Catharine L. Smith

Epigenetics ◽  
2009 ◽  
Vol 4 (8) ◽  
pp. 577-586 ◽  
Author(s):  
Lina Fassi Fehri ◽  
Cindy Rechner ◽  
Sabrina Janßen ◽  
Tim Nam Mak ◽  
Carsten Holland ◽  
...  

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Kyle H. Bond ◽  
Jennifer L. Fetting ◽  
Christine W. Lary ◽  
Ivette F. Emery ◽  
Leif Oxburgh

Abstract Background Forkhead transcription factors control cell growth in multiple cancer types. Foxd1 is essential for kidney development and mitochondrial metabolism, but its significance in renal cell carcinoma (ccRCC) has not been reported. Methods Transcriptome data from the TCGA database was used to correlate FOXD1 expression with patient survival. FOXD1 was knocked out in the 786-O cell line and known targets were analyzed. Reduced cell growth was observed and investigated in vitro using growth rate and Seahorse XF metabolic assays and in vivo using a xenograft model. Cell cycle characteristics were determined by flow cytometry and immunoblotting. Immunostaining for TUNEL and γH2AX was used to measure DNA damage. Association of the FOXD1 pathway with cell cycle progression was investigated through correlation analysis using the TCGA database. Results FOXD1 expression level in ccRCC correlated inversely with patient survival. Knockout of FOXD1 in 786-O cells altered expression of FOXD1 targets, particularly genes involved in metabolism (MICU1) and cell cycle progression. Investigation of metabolic state revealed significant alterations in mitochondrial metabolism and glycolysis, but no net change in energy production. In vitro growth rate assays showed a significant reduction in growth of 786-OFOXD1null. In vivo, xenografted 786-OFOXD1null showed reduced capacity for tumor formation and reduced tumor size. Cell cycle analysis showed that 786-OFOXD1null had an extended G2/M phase. Investigation of mitosis revealed a deficiency in phosphorylation of histone H3 in 786-OFOXD1null, and increased DNA damage. Genes correlate with FOXD1 in the TCGA dataset associate with several aspects of mitosis, including histone H3 phosphorylation. Conclusions We show that FOXD1 regulates the cell cycle in ccRCC cells by control of histone H3 phosphorylation, and that FOXD1 expression governs tumor formation and tumor growth. Transcriptome analysis supports this role for FOXD1 in ccRCC patient tumors and provides an explanation for the inverse correlation between tumor expression of FOXD1 and patient survival. Our findings reveal an important role for FOXD1 in maintaining chromatin stability and promoting cell cycle progression and provide a new tool with which to study the biology of FOXD1 in ccRCC.


2017 ◽  
Vol 28 ◽  
pp. 96-105 ◽  
Author(s):  
Xia Wu ◽  
Jing Wang ◽  
Yuqin Shi ◽  
Sai Chen ◽  
Qiaojuan Yan ◽  
...  

2006 ◽  
Vol 101 (3) ◽  
pp. 697-708 ◽  
Author(s):  
Karen Brami-Cherrier ◽  
Jeremie Lavaur ◽  
Christiane Pagès ◽  
J. Simon C. Arthur ◽  
Jocelyne Caboche

BMC Cancer ◽  
2011 ◽  
Vol 11 (1) ◽  
Author(s):  
Chien-Chih Lee ◽  
Yi-Hsiung Lin ◽  
Wen-Hsin Chang ◽  
Pei-Chin Lin ◽  
Yang-Chang Wu ◽  
...  

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