THOMAS KING

Office: Copernicus 204
Lab: Copernicus 429 (Animal Suite) 860-832-2654
kingt@ccsu.edu

Courses Taught:

Research Interests:

My research interests concern the genetic analysis of development in mammals, using mice and rats as model mammalian systems. With the long-term goal of gaining access to the molecular biology underlying interesting mutant phenotypes, my work prior to my appointment at CCSU produced a number of high-resolution genetic maps including genomic regions on mouse Chromosomes 7, 10, 17 and the Y Chromosome. At CCSU, my laboratory has investigated a novel mutation in rats (designated shorn) that causes recessive alopecia (Moemeka et al., J. Heredity 89, 257-260; Hall et al., J. Heredity 91, 345-347; Chrissluis et al., 2002, Molecular Genetics and Metabolism, 76, 335-339), and we have made progress mapping the X-linked histoincompatibility locus (Alner et al., Immunogenetics 55, 87-94). We are currently pursuing three different projects:

  1. We are investigating the molecular genetic basis of a pleiotropic developmental mutation in the mouse, designated mshi. This mutation controls recessive male sterility, and loss of an unusual new type of histocompatibility locus that is detected in vivo by helper T cells. We have mapped this mutation to mouse Chr 10 (Turner et al., Genomics 39, 1-7; Rule et al., Mammalian Genome 10, 447-450), and have made progress characterizing both the histocompatibility (Hildebrandt et al., Immunogenetics 49, 666-672) and reproductive aspects of the mutant phenotype. We have also investigated the occurrence of programmed cell death (apoptosis) in mutant gonads, vs. wild type (in collaboration with James Mulrooney, CCSU). We have recently discovered that Mtap7 is the gene disrupted by the mshi mutation (Magnan et al., Molecular Genetics and Metabolism 97, 155-162). Further studies of the Mtap7mshi allele will be supported by an AREA grant through 2010.
  2. Another project, the mapping of the Charles River “hairless” mutation, was started in Fall, 2001 (Ahearn et al., J. Heredity 93, 210-213). This work suggested Fgfr2 as a possible gene candidate for the Charles River “hairless” mutation, which we also showed is an allele of rat fuzzy and a likely orthologue of mouse frizzy. Our research has created a high-resolution map for the mouse fr mutation (Paul et al., Experimental Dermatology, 17, 640-644), which has facilitated the identification of the single base-pair change in the Prss8 gene that causes the mutant fr phenotype (Spacek et al., Experimental Dermatology, in press). We have also found a 12-basepair deletion in the Prss8 gene in hairless rats, and expect to find a Prss8 defect in the fuzzy rat as well. An AREA grant will support this work through 2010.
  3. We are initiating a new positional cloning program, which will aim to identify the gene mutated in a set of 6 mutants with mutations that affect hair development. Analysis of large backcrosses segregating for wooly (wly) and juvenile alopecia (jal) are currently in progress.

Publications (CCSU student authors are underlined):

deco dividing bar

 

Return to the BMS Faculty Page

Return to the CCSU Biomolecular Sciences Department home page

Revised December 15, 2009