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Article

Accumulation and Phosphorylation of RecQ-Mediated Genome Instability Protein 1 (RMI1) at Serine 284 and Serine 292 during Mitosis

by 1,†, 1,†, 1, 1, 1, 1, 1,* and 2,*
1
Tianjin Key Laboratory of Radiation Medicine and Molecular Nuclear Medicine, Institute of Radiation Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300192, China
2
Department of Experimental Radiation Oncology, the University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editor: Alan C. Leonard
Int. J. Mol. Sci. 2015, 16(11), 26395-26405; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms161125965
Received: 15 September 2015 / Revised: 22 October 2015 / Accepted: 26 October 2015 / Published: 4 November 2015
(This article belongs to the Special Issue Molecular Machinery of Cell Growth Regulation)
Chromosome instability usually leads to tumorigenesis. Bloom syndrome (BS) is a genetic disease associated with chromosome instability. The BS gene product, BLM, has been reported to function in the spindle assembly checkpoint (SAC) to prevent chromosome instability. BTR complex, composed of BLM, topoisomerase IIIα (Topo IIIα), RMI1 (RecQ-mediated genome instability protein 1, BLAP75) and RMI2 (RecQ-mediated genome instability protein 2, BLAP18), is crucial for maintaining genome stability. Recent work has demonstrated that RMI2 also plays critical role in SAC. However, little is know about RMI1 regulation during the cell cycle. Here we present that RMI1 protein level does not change through G1, S and G2 phases, but significantly increases in M phase. Moreover, phosphorylation of RMI1 occurs in mitosis. Upon microtubule-disturbing agent, RMI1 is phosphorylated primarily at the sites of Serine 284 and Serine 292, which does not interfere with the formation of BTR complex. Additionally, this phosphorylation is partially reversed by roscovitine treatment, implying cycling-dependent kinase 1 (CDK1) might be one of the upstream kinases. View Full-Text
Keywords: RMI1 (RecQ-mediated genome instability protein 1); BTR (BLM-Topo IIIα-RMI) complex; mitosis; phosphorylation RMI1 (RecQ-mediated genome instability protein 1); BTR (BLM-Topo IIIα-RMI) complex; mitosis; phosphorylation
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MDPI and ACS Style

Xu, C.; Wang, Y.; Wang, L.; Wang, Q.; Du, L.-Q.; Fan, S.; Liu, Q.; Li, L. Accumulation and Phosphorylation of RecQ-Mediated Genome Instability Protein 1 (RMI1) at Serine 284 and Serine 292 during Mitosis. Int. J. Mol. Sci. 2015, 16, 26395-26405. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms161125965

AMA Style

Xu C, Wang Y, Wang L, Wang Q, Du L-Q, Fan S, Liu Q, Li L. Accumulation and Phosphorylation of RecQ-Mediated Genome Instability Protein 1 (RMI1) at Serine 284 and Serine 292 during Mitosis. International Journal of Molecular Sciences. 2015; 16(11):26395-26405. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms161125965

Chicago/Turabian Style

Xu, Chang, Yan Wang, Lu Wang, Qin Wang, Li-Qing Du, Saijun Fan, Qiang Liu, and Lei Li. 2015. "Accumulation and Phosphorylation of RecQ-Mediated Genome Instability Protein 1 (RMI1) at Serine 284 and Serine 292 during Mitosis" International Journal of Molecular Sciences 16, no. 11: 26395-26405. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms161125965

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