International Mammalian Genome Society

The 15th International Mouse Genome Conference (2001)


Prof Karen Artzt
University of Texas at Austin
Institute for Cellular and Molecular Biology
Section of Molecular Genetics and Microbiology; A4800
Austin 78712-1064 USA

Co-Authors: Wu J, Centilli M, Vasquez G, Young S, Scolnick J, Spearow JL
Institution:   University of Texas at Austin Institute for Cellular and Molecular Biology, University of California at Davis

During a microsatellite genome scan to map tint (T/t tail interaction factor), we discovered a new hypomorphic gene that suppresses the Brachyury (T)phenotype.  Homozygotes for the T/T die of serious axis defects on E10.5 while heterozygotes have a short tail.  Double heterozygosity for both T and SuB have normal tails. To our knowledge, this is the first gene that improves axis defects and therefore may be relevant to spina bifida.

The origin for Sub is a spretus subline that was used in our intercross (Spr/Jls-RP):  F1 mice were wild type at the T locus and heterozygous for tint versus spretus. Since all the F1s were normal tailed, to monitor the transmission of tint, it was necessary to testcross to T/+, +/+.  We expected 1/2 normal tails, 1/4 shorts (T/+, spretus/+) and 1/4 tailless (T/+, tint/+) offspring.  The normal tails would be of two indistinguishable genotypes and were discarded.  In 713 testcross progeny, instead of the expected 2:1:1 ratio, we found a 2.5:1:0.5 ratio.  When markers on chromosome 6 were typed, virtually all the tailless mice were of the tint type.  The exceptions were recombinants for neighboring markers.  The data map SuB to spretus chromosome 6 at 35.22 cM inseparable from D6Mit22 but distinct from D6Mit386.  When T/+ was crossed to the input spretus stock, in the absence of any interaction, half the progeny are expected to be short tailed. The fact that 59/59 progeny had normal tails argues that we identified a suppressor of T.

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