HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (16) Citing Articles via Google Scholar Google Scholar Articles by Palijan, A. Articles by Deng, A. Y. Search for Related Content PubMed PubMed Citation Articles by Palijan, A. Articles by Deng, A. Y.

Quantitative trait loci with opposing blood pressure effects demonstrating epistasis on Dahl rat chromosome 3

Research Centre-Centre Hospitalier de l’Université de Montreal CHUM, Hôtel Dieu, Montreal, Quebec H2W 1T8, Canada

Our previous linkage studies indicated that there might be a blood pressure (BP) quantitative trait locus (QTL) on chromosome 3 (Chr 3) contrasting between the Dahl salt-sensitive (S) strain and the Lewis (LEW) strain. To prove and then to narrow down the segment containing this QTL, five congenic strains have been generated by replacing various segments of the S rats with the homologous segments of the LEW rats. They are designated as S.L1, S.L2, S.L3, S.L4, and S.L5, respectively. S.L2, S.L3, S.L4, and S.L5 are substrains of S.L1, i.e., they contain substitutions of smaller sections within the large fragment defined by S.L1. The construction of these congenic strains was facilitated by a genome-wide marker screening process. BPs of the rats were measured by telemetry. S.L2 and S.L3 shared a fragment of Chr 3 in common and both showed a BP-lowering effect, indicating the existence of "-BP" QTL alleles from LEW compared with S. In contrast, S.L4 involves a section with no overlap with either S.L2 or S.L3, and S.L4 showed a BP significantly higher than that of S rats, indicating the presence of "+BP" QTL alleles from LEW compared with S. Interestingly, the combined effect of the -BP QTL and +BP QTL alleles was "-" in S.L1, implying that the "-" QTL is epistatic to "+" QTL.

genetic hypertension; rat chromosome 3; Lewis rat; congenic strains

This article has been cited by other articles:

				C. Moreno, M. L. Kaldunski, T. Wang, R. J. Roman, A. S. Greene, J. Lazar, H. J. Jacob, and A. W. Cowley Jr. Multiple blood pressure loci on rat chromosome 13 attenuate development of hypertension in the Dahl S hypertensive rat Physiol Genomics, October 19, 2007; 31(2): 228 - 235. [Abstract] [Full Text] [PDF]

				A. Y. Deng Genetic basis of polygenic hypertension Hum. Mol. Genet., October 15, 2007; 16(R2): R195 - R202. [Abstract] [Full Text] [PDF]

				A. Y. Deng Positional Cloning of Quantitative Trait Loci for Blood Pressure: How Close Are We?: A Critical Perspective Hypertension, April 1, 2007; 49(4): 740 - 747. [Full Text] [PDF]

				S. J. Lee, J. Liu, A. M. Westcott, J. A. Vieth, S. J. DeRaedt, S. Yang, B. Joe, and G. T. Cicila Substitution Mapping in Dahl Rats Identifies Two Distinct Blood Pressure Quantitative Trait Loci Within 1.12- and 1.25-Mb Intervals on Chromosome 3 Genetics, December 1, 2006; 174(4): 2203 - 2213. [Abstract] [Full Text] [PDF]

				S. Charron, R. Lambert, V. Eliopoulos, C. Duong, A. Menard, J. Roy, and A. Y. Deng A loss of genome buffering capacity of Dahl salt-sensitive model to modulate blood pressure as a cause of hypertension Hum. Mol. Genet., December 15, 2005; 14(24): 3877 - 3884. [Abstract] [Full Text] [PDF]

				S. Charron, C. Duong, A. Menard, J. Roy, V. Eliopoulos, R. Lambert, and A. Y. Deng Epistasis, Not Numbers, Regulates Functions of Clustered Dahl Rat Quantitative Trait Loci Applicable to Human Hypertension Hypertension, December 1, 2005; 46(6): 1300 - 1308. [Abstract] [Full Text] [PDF]

				V. Eliopoulos, J. Dutil, Y. Deng, M. Grondin, and A. Y. Deng Severe hypertension caused by alleles from normotensive Lewis for a quantitative trait locus on chromosome 2 Physiol Genomics, June 16, 2005; 22(1): 70 - 75. [Abstract] [Full Text] [PDF]

				J. Dutil, V. Eliopoulos, E.-L. Marchand, A. M. Devlin, J. Tremblay, K. Prithiviraj, P. Hamet, A. Migneault, D. deBlois, and A. Y. Deng A quantitative trait locus for aortic smooth muscle cell number acting independently of blood pressure: implicating the angiotensin receptor AT1B gene as a candidate Physiol Genomics, May 11, 2005; 21(3): 362 - 369. [Abstract] [Full Text] [PDF]

				M. W. McBride, M. J. Brosnan, J. Mathers, L. I. McLellan, W. H. Miller, D. Graham, N. Hanlon, C. A. Hamilton, J. M. Polke, W. K. Lee, et al. Reduction of Gstm1 Expression in the Stroke-Prone Spontaneously Hypertension Rat Contributes to Increased Oxidative Stress Hypertension, April 1, 2005; 45(4): 786 - 792. [Abstract] [Full Text] [PDF]

				J. Dutil, V. Eliopoulos, J. Tremblay, P. Hamet, S. Charron, and A. Y. Deng Multiple Quantitative Trait Loci for Blood Pressure Interacting Epistatically and Additively on Dahl Rat Chromosome 2 Hypertension, April 1, 2005; 45(4): 557 - 564. [Abstract] [Full Text] [PDF]

				M. Grondin, V. Eliopoulos, R. Lambert, Y. Deng, A. Ariyarajah, M. Moujahidine, J. Dutil, S. Charron, and A. Y. Deng Complete and overlapping congenics proving the existence of a quantitative trait locus for blood pressure on Dahl rat chromosome 17 Physiol Genomics, March 21, 2005; 21(1): 112 - 116. [Abstract] [Full Text] [PDF]

				C. A. Mein, M. J. Caulfield, R. J. Dobson, and P. B. Munroe Genetics of essential hypertension Hum. Mol. Genet., April 1, 2004; 13(90001): R169 - 175. [Abstract] [Full Text] [PDF]