Further studies on knockout mice lacking a functional dynein heavy chain (MDHC7).: 1.: Evidence for a structural deficit in the axoneme

被引:15
作者
Vernon, GG
Neesen, J
Woolley, DM
机构
[1] Univ Bristol, Sch Med Sci, Dept Physiol, Bristol BS8 1TD, Avon, England
[2] Univ Gottingen, Inst Human Genet, D-3400 Gottingen, Germany
来源
CELL MOTILITY AND THE CYTOSKELETON | 2005年 / 61卷 / 02期
关键词
axoneme; inner dynein arms; sperm motility; deep etch; electron microscopy;
D O I
10.1002/cm.20066
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Male mice had previously been generated in which the inner dynein arm heavy chain 7 gene (MDHC7) was inactivated by the substitution of four exons encoding the ATP-binding site (PI-loop) with the neomycin resistance gene, giving a putative non-functional gene product. We have used additional techniques Of electron microscopy to determine what effect the truncated, non-functional heavy chain has on the assembly of the inner dynein arm complex. From a comparison of MDHC7-/- with the wild-type morphology, we have found that the expected loss of a C-terminal (globular) domain is associated with inner dynein arm 3, a change from two visible "heads" to one. This deficit was seen in replicas of rapidly-frozen, deeply-etched spermatozoa, and was confirmed in filtered images of 20-nm-thin sections, cut in longitudinal planes. Assembly of the other IDAs appeared unaffected. This study is the first to reveal the location of a specific dynein heavy chain within the 96-nm repeat pattern of the inner dynein arms of the mammalian axoneme. Cell Motil. Cytoskeleton 61:65-73, 2005. (c) 2005 Wiley-Liss, Inc.
引用
收藏
页码:65 / 73
页数:9
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