HIGH POSTNATAL LETHALITY AND TESTIS DEGENERATION IN RETINOIC ACID RECEPTOR-ALPHA MUTANT MICE

被引：492

作者：

LUFKIN, T ^{[1
]}

LOHNES, D ^{[1
]}

MARK, M ^{[1
]}

DIERICH, A ^{[1
]}

GORRY, P ^{[1
]}

GAUB, MP ^{[1
]}

LEMEUR, M ^{[1
]}

CHAMBON, P ^{[1
]}

机构：

[1] FAC MED STRASBOURG,INSERM,UNITE BIOL MOLEC & GENIE GENET 184,CNRS,GENET MOLEC EUCARYOTES LAB,F-67085 STRASBOURG,FRANCE

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 1993年 / 90卷 / 15期

关键词：

VITAMIN-A; GENE TARGETING; SPERMATOGENESIS;

D O I：

10.1073/pnas.90.15.7225

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Retinoic acid (RA) plays a critical role in normal development, growth, and maintenance of certain tissues. The action of RA is thought to be mediated in part by the three nuclear receptors (RARalpha, -beta, and -gamma), each of which is expressed as multiple isoforms. To investigate the function of the RARalpha gene, we have disrupted, in the mouse, the whole gene or the isoform RARalpha1. Although RARalpha1 is the predominant isoform and is highly conserved among vertebrates, RARalpha1-null mice appeared normal. However, targeted disruption of the whole RARalpha gene resulted in early postnatal lethality and testis degeneration. These results, showing that RARalpha is indeed involved in the transduction of the RA signal, also suggest an unexpected genetic redundancy.

引用

页码：7225 / 7229

页数：5

共 46 条

[1]

BROOKFIELD J, 1992, EVOL GENET, V2, P553

[2] ALTERING THE GENOME BY HOMOLOGOUS RECOMBINATION [J].