Mutations in the first intron of the SHR renin gene disrupt putative regulatory elements.
1. Four single base mutations unique to the spontaneously hypertensive rat (SHR) were identified in the first 1100 base pairs of its renin gene first intron when compared to that of Wistar-Kyoto and Sprague-Dawley normotensive rats. 2. These mutations were found to fall within the consensus sequences for a number of transcription factors and thus may alter the affinity of these putative transcription factor binding sites. 3. The reported overexpression of the renin gene in the SHR may therefore result from these structural abnormalities and, in turn, result in a tissue angiotensin-dependent hypertension in this strain.
Yu
H
H
Department of Physiology, University of Melbourne, Parkville, Victoria, Australia.
Di Nicolantonio
R
R
Lan
L
L
Wilks
A
A
D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D001483:Base Sequence; D001665:Binding Sites; D016384:Consensus Sequence; D017931:DNA Primers / Q000737:chemistry; D004195:Disease Models, Animal; D005786:Gene Expression Regulation / Q000235:genetics; D006973:Hypertension / Q000235:genetics*; D007438:Introns / Q000235:genetics*; D008099:Liver / Q000378:metabolism; D008969:Molecular Sequence Data; D017354:Point Mutation / Q000235:genetics*; D012326:RNA Splicing / Q000235:genetics; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D017207:Rats, Sprague-Dawley; D012083:Renin / Q000235:genetics*; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism
D017931:DNA Primers; D014157:Transcription Factors; D000804:Angiotensin II; D012083:Renin