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
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.