Loss of REEP4 causes paralysis of the Xenopus embryo

被引:10
作者
Argasinska, Joanna
Rana, Amer A.
Gilchrist, Michael J.
Lachani, Kim
Young, Alice
Smith, James C. [1 ]
机构
[1] Univ Cambridge, Wellcome Trust Canc Res UK Gurdon Inst, Cambridge CB2 1QN, England
基金
英国惠康基金; 英国生物技术与生命科学研究理事会;
关键词
Xenopus; REEP4; neural; muscle; YEAST HOMOLOG; GENE; EXPRESSION; MUSCLE; MUTATIONS; PROTEIN; MYOD; ACTIVATION; INDUCTION; MEMBERS;
D O I
10.1387/ijdb.072542ja
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Members of the REEP (Receptor expression enhancing protein) family contain a TB2/DP1, HVA22 domain that is involved in intracellular trafficking and secretion. Consistent with the presence of this domain, REEP1 and REEP3 enhance the expression of odorant and taste receptors in mammals, while mutation of these genes causes defects in neural development. REEP4 was identified in the course of a functional antisense morpholino oligonucleotide screen searching for genes involved in the early development of Xenopus tropicalis: although over-expression of the gene causes no phenotype, embryos lacking REEP4 develop a slightly kinked body axis and are paralysed. At tailbud stages of development, REEP4 is expressed in the somites and neural tube. The paralysis observed in embryos lacking REEP4 might therefore be caused by defects in the nervous system or in muscle. To address this point, we examined the expression of various neural and muscle markers and found that although all are expressed normally at early stages of development, many are down regulated by the tailbud stage. This suggests that REEP4 plays a role in the maintenance of both the nervous system and the musculature.
引用
收藏
页码:37 / 43
页数:7
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