Abstract
Aurora kinase B regulates the segregation of chromosomes and the spindle checkpoint during mitosis. In this study, we showed that the Microprocessor complex, which is responsible for the processing of the primary transcripts during the generation of microRNAs, destabilizes the mRNA of Aurora kinase B in human cells. The Microprocessor-mediated cleavage kept Aurora kinase B at a low level and prevented premature entrance into mitosis. The cleavage was reduced during mitosis leading to the accumulation of Aurora kinase B mRNA and protein. In addition to Aurora kinase B mRNA, the processing of other primary transcripts of miRNAs were also decreased during mitosis. We found that the cleavage was dependent on an RNA helicase, DDX5, and the association of DDX5 and DDX17 with the Microprocessor was reduced during mitosis. Thus, we propose a novel mechanism by which the Microprocessor complex regulates stability of Aurora kinase B mRNA and cell cycle progression.
| Original language | English |
|---|---|
| Pages (from-to) | 241-247 |
| Number of pages | 7 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 446 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2014 Mar 28 |
Fingerprint
Keywords
- Aurora kinase B
- Cell cycle
- Mitosis
- The Microprocessor complex
ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Cell Biology
- Molecular Biology
Cite this
Cell cycle-dependent regulation of Aurora kinase B mRNA by the Microprocessor complex. / Jung, Eunsun; Seong, Youngmo; Seo, Jae Hong; Kwon, Young Soo; Song, Hoseok.
In: Biochemical and Biophysical Research Communications, Vol. 446, No. 1, 28.03.2014, p. 241-247.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Cell cycle-dependent regulation of Aurora kinase B mRNA by the Microprocessor complex
AU - Jung, Eunsun
AU - Seong, Youngmo
AU - Seo, Jae Hong
AU - Kwon, Young Soo
AU - Song, Hoseok
PY - 2014/3/28
Y1 - 2014/3/28
N2 - Aurora kinase B regulates the segregation of chromosomes and the spindle checkpoint during mitosis. In this study, we showed that the Microprocessor complex, which is responsible for the processing of the primary transcripts during the generation of microRNAs, destabilizes the mRNA of Aurora kinase B in human cells. The Microprocessor-mediated cleavage kept Aurora kinase B at a low level and prevented premature entrance into mitosis. The cleavage was reduced during mitosis leading to the accumulation of Aurora kinase B mRNA and protein. In addition to Aurora kinase B mRNA, the processing of other primary transcripts of miRNAs were also decreased during mitosis. We found that the cleavage was dependent on an RNA helicase, DDX5, and the association of DDX5 and DDX17 with the Microprocessor was reduced during mitosis. Thus, we propose a novel mechanism by which the Microprocessor complex regulates stability of Aurora kinase B mRNA and cell cycle progression.
AB - Aurora kinase B regulates the segregation of chromosomes and the spindle checkpoint during mitosis. In this study, we showed that the Microprocessor complex, which is responsible for the processing of the primary transcripts during the generation of microRNAs, destabilizes the mRNA of Aurora kinase B in human cells. The Microprocessor-mediated cleavage kept Aurora kinase B at a low level and prevented premature entrance into mitosis. The cleavage was reduced during mitosis leading to the accumulation of Aurora kinase B mRNA and protein. In addition to Aurora kinase B mRNA, the processing of other primary transcripts of miRNAs were also decreased during mitosis. We found that the cleavage was dependent on an RNA helicase, DDX5, and the association of DDX5 and DDX17 with the Microprocessor was reduced during mitosis. Thus, we propose a novel mechanism by which the Microprocessor complex regulates stability of Aurora kinase B mRNA and cell cycle progression.
KW - Aurora kinase B
KW - Cell cycle
KW - Mitosis
KW - The Microprocessor complex
UR - http://www.scopus.com/inward/record.url?scp=84898013887&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84898013887&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2014.02.104
DO - 10.1016/j.bbrc.2014.02.104
M3 - Article
VL - 446
SP - 241
EP - 247
JO - The BMJ
JF - The BMJ
SN - 0730-6512
IS - 1
ER -