Cell-cycle regulation of the p53-inducible gene B99

被引:39
作者
Collavin, L
Monte, M
Verardo, R
Pfleger, C
Schneider, C
机构
[1] Lab Nazl Consorzio Interuniv Biotecnol, I-34012 Trieste, Italy
[2] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA
[3] Univ Udine, Dipartimento Sci & Tecnol Biomed, I-33100 Udine, Italy
关键词
B99; p53-inducible gene; cell cycle; G2; phase-specific; Gtse-1;
D O I
10.1016/S0014-5793(00)01969-4
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
B99 is a p53-inducible gene whose accumulation upon p53 activation is restricted to late S/G2 cells. Here we have analyzed B99 regulation during the cell cycle in murine cells with or without functional p53, We report that B99 accumulates in late S/G2 phase, is phosphorylated in mitosis, and disappears in G1 phase, regardless of the status of p53. As a complement to this observation, we show: that B99 is not induced by p53 in quiescent cells. Therefore, B99 expression is modulated both by cell-cycle regulatory mechanisms and by p53, and p53 can increase the cellular levels of B99 only during the window of the cell cycle when it is normally expressed, On the basis of these observations we rename B99 Gtse-1 (G-two- and S-phase-expressed), (C) 2000 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:57 / 62
页数:6
相关论文
共 45 条
[1]   P53 CONTROLS BOTH THE G(2)/M AND THE G(1) CELL-CYCLE CHECKPOINTS AND MEDIATES REVERSIBLE GROWTH ARREST IN HUMAN FIBROBLASTS [J].
AGARWAL, ML ;
AGARWAL, A ;
TAYLOR, WR ;
STARK, GR .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (18) :8493-8497
[2]   Regulation of p21cip1 expression by growth factors and the extracellular matrix reveals a role for transient ERK activity in G1 phase [J].
Bottazzi, ME ;
Zhu, XY ;
Böhmer, RM ;
Assoian, RK .
JOURNAL OF CELL BIOLOGY, 1999, 146 (06) :1255-1264
[3]   The proteolysis of mitotic cyclins in mammalian cells persists from the end of mitosis until the onset of S phase [J].
Brandeis, M ;
Hunt, T .
EMBO JOURNAL, 1996, 15 (19) :5280-5289
[4]   BOTH VIRAL (ADENOVIRUS E1B) AND CELLULAR (HSP-70, P53) COMPONENTS INTERACT WITH CENTROSOMES [J].
BROWN, CR ;
DOXSEY, SJ ;
WHITE, E ;
WELCH, WJ .
JOURNAL OF CELLULAR PHYSIOLOGY, 1994, 160 (01) :47-60
[5]   A P53-DEPENDENT MOUSE SPINDLE CHECKPOINT [J].
CROSS, SM ;
SANCHEZ, CA ;
MORGAN, CA ;
SCHIMKE, MK ;
RAMEL, S ;
IDZERDA, RL ;
RASKIND, WH ;
REID, BJ .
SCIENCE, 1995, 267 (5202) :1353-1356
[6]  
DAVIS FM, 1983, P NATL ACAD SCI-BIOL, V80, P2926, DOI 10.1073/pnas.80.10.2926
[7]   THE GROWTH ARREST-SPECIFIC GENE, GAS1, IS INVOLVED IN GROWTH SUPPRESSION [J].
DELSAL, G ;
RUARO, ME ;
PHILIPSON, L ;
SCHNEIDER, C .
CELL, 1992, 70 (04) :595-607
[8]  
DelSal G, 1996, ONCOGENE, V12, P177
[9]  
DELSAL G, 1995, MOL CELL BIOL, V15, P7152
[10]   MICE LACKING P21(C/P1/WAF1) UNDERGO NORMAL DEVELOPMENT, BUT ARE DEFECTIVE IN G1 CHECKPOINT CONTROL [J].
DENG, CX ;
ZHANG, PM ;
HARPER, JW ;
ELLEDGE, SJ ;
LEDER, P .
CELL, 1995, 82 (04) :675-684