Professor, Departments of Molecular and Human Genetics and Neuroscience

B.A., Fort Lewis College, 1986
M.A., University of Colorado, 1988
Ph.D., University of Colorado, 1991
Postdoc, Institute for Behavioral Genetics, University of Colorado, 1993
Postdoc, National Institute of Mental Health, 1998
Sen. Staff Fellow, National Institute of Mental Health, NIH, 1998

RESEARCH INTERESTS:

The lab's primary interest is in using mouse genetic models to understand mental retardation and developmental disabilities. Fragile X syndrome (FXS) is the most common inherited cause of human mental retardation with an estimated prevalence of 1 in 4,000 males. Together with several physical features, individuals with FXS display a number of behavioral abnormalities including cognitive impairment, hyperactivity, attention deficits, sensory hypersensitivity and hyperarousal, social isolation and anxiety, and autistic-like behaviors. FXS results from the loss of expression of the Fragile X mental retardation (FMR1) gene located on the X-chromosome. Fmr1 knockout (KO) mice, which have undetectable levels of Fmr1 mRNA and the FMRP protein, exhibit several of the physical and behavioral characteristics of the human syndrome. Interestingly, there is significant variability in the presence and expression of the behavioral abnormalities in FXS. Our lab is interested in understanding the nature of the behavioral abnormalities in FXS by systematically evaluating numerous behavioral responses of Fmr1 KO mice on assays for anxiety, hyperactivity, social interactions, and learning and memory. In addition, we are testing the hypothesis that the variability in FXS results from differences in genetic background, the home environment and their interaction by examining the impact of genetic background (G), rearing environment (E), and the interaction of G X E on the behavior of Fmr1 KO mice. Finally, we are evaluating the potential for using the Fmr1 KO mouse as a model system for identifying potential therapeutic interventions for FXS.

Huntington's disease (HD) constitutes a CAG triplet repeat genetic disorder resulting in neurodegeneration. The mutation creates an expanded polyglutamine stretch in the huntingtin protein. Although most researchers are aware that individuals with HD display abnormal motor responses, the clinical presentation of HD also encompasses cognitive and psychiatric symptoms. Of particular interest is the fact that signs of cognitive and psychiatric dysfunction can precede the motor impairments. Therefore, gaining insight into the nature of the cognitive and psychiatric as well as the motor dysfunction of HD is critical to understanding the disease pathogenesis and to developing more appropriate therapeutic interventions. Although many individuals with HD display similar neurological symptoms, they are not necessarily identical. The long-term goal of this project is to employ the R6/2 transgenic mice to identify putative genetic/molecular modifiers of HD, which could lead to potential targets for therapeutic intervention.

SELECTED PUBLICATIONS:

1. Hou L, Antion MD, Spencer CM, Paylor R, Klann E (2006). Dynamic translational and proteasomal regulation of the Fragile X mental retardation protein controls metabotropic glutamate receptor-dependent long-term depression. Neuron 51: 441-454.

2. Walz K, Paylor R, Yan J, Bi W, Lupski JR (2006). Rai1 duplication causes physical and behavioral phenotypes in a mouse model for dup(17)(p11.2p11.2). J. Clin. Invest. 116: 3035-3041.

3. Spencer CM, Serysheva E, Yuva-Paylor LA, Oostra BA, Nelson DL, Paylor R (2006). Exaggerated behavioral phenotypes in Fmr1/Fxr2 double knockout mice reveal a functional genetic interaction between Fragile X-related proteins. Hum. Mol. Genet. 15: 1984-1994.

4. Paylor R, Glaser B, Mupo A, Ataliotis P, Spencer C, Sobotka A, Sparks C, Choi CH, Oghalai J, Curran S, Murphy K, Williams N, O'Donovan M, Owen MJ, Scrambler PJ, Lindsay E (2006). Tbx1 haploinsufficiency is linked to behavioral disorders in mice and humans: Implications for 22q11 deletion syndrome. Proc. Natl. Acad. Sci. USA 103: 7729-7734.

5. Brennan FX, Albeck DS, Paylor R (2006). Fmr1 knockout mice are impaired in a leverpress escape/avoidance task. Genes Brain Behav. 5: 467-471.

6. Paylor R, Spencer CM, Yuva-Paylor LA, Pieke-Dahl S (2006). The use of behavioral test batteries, II: Effect of test interval. Physiol. Behav. 87: 95-102.

7. Spencer CM, Alekseyenko O, Serysheva K, Yuva-Paylor LA, Paylor R (2005). Altered anxiety-related and social behaviors in the Fmr1 knockout mouse model of fragile X syndrome. Genes Brain Behav. 4: 420-430.

8. Bouwknecht JA, van der Gugten J, Groenink L, Olivier B, Paylor R (2004). Effects of repeated testing in two inbred strains on flexinoxan dose-response curves in three mouse models for anxiety. Euro. J. Pharmacol. 494: 35-44.

For more publications, see listing on Pub Med.

CONTACT INFORMATION:

Richard E. Paylor, Ph.D.
Department of Molecular and Human Genetics
Baylor College of Medicine
One Baylor Plaza
Houston, TX 77030, U.S.A.
Mail Stop: NAB 2015

Phone: 713-798-6124
Fax: 713-798-5386
E-mail:

Community of Science Expertise Record: 356544 This will take you to the COS website. Use the "Back" button on your browser to return to this site.

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