Physical mapping of male fertility and meiotic drive quantitative trait loci in the mouse t complex using chromosome deficiencies

Citation
A. Planchart et al., Physical mapping of male fertility and meiotic drive quantitative trait loci in the mouse t complex using chromosome deficiencies, GENETICS, 155(2), 2000, pp. 803-812
Citations number
40
Categorie Soggetti
Biology,"Molecular Biology & Genetics
Journal title
GENETICS
ISSN journal
00166731 → ACNP
Volume
155
Issue
2
Year of publication
2000
Pages
803 - 812
Database
ISI
SICI code
0016-6731(200006)155:2<803:PMOMFA>2.0.ZU;2-C
Abstract
The t complex spans 20 cM of the proximal region of mouse chromosome 17. A variant form, the t haplotype (t), exists at significant frequencies in wil d mouse populations and is characterized by the presence of inversions that suppress recombination with Mild-type (+) chromosomes. Transmission ratio distortion and sterility are associated with t and affect males only. It is hypothesized that these phenomena are caused by trans-acting distorter/ste rility factors that interact with a responder locus (Tcr(t)) and that the d istorter and sterility factors are the same because homozygosity of the dis torters causes male sterility. One factor, Tcd1, was previously shown to be amorphic using a chromosome deletion. To overcome limitations imposed by r ecombination suppression, we used a series of deletions within the t comple x in trans to t chromosomes to characterize the Tcd1 region. The find that the distorter activity of Tcd1 is distinct from a linked sterility factor, originally called tcs1. YACs mapped with respect to deletion breakpoints lo calize tcs1 to a 1.1-Mb interval flanked by D17Aus9 and Tctex1. We present evidence for the existence of multiple proximal t complex regions that exhi bit distorter activity. These studies demonstrate the utility of chromosome deletions for complex trait analysis.