All Phenotypes Rgs2<tm1Pngr> MGI Mouse

behavior/neurological phenotype ( J:77273 )

N	• homozygous null mice displayed no apparent defects in motor responses, circadian activity, exploratory behavior, motor coordination, or spatial learning and memory

decreased aggression ( J:77273 )

• homozygous mutant male mice displayed significantly reduced aggressive behavior compared with their heterozygous littermates; in contrast, the aggressive behavior of homozygous mutant female mice appeared normal

increased anxiety-related response ( J:77273 )

• when subjected to the light/dark preference test, mutant mice showed a greater preference for the dark compared with heterozygous control littermates, indicating increased anxiety

• in addition, mutant mice showed an elevated response to acoustic startling

cardiovascular system phenotype ( J:86774 )

N

• homozygous mutant mice exhibited no significant differences in heart rate compared with wild-type littermates

• at 3-4 months, homozygous mutant mice showed normal body, kidney and heart weights, as well as normal ratios of heart or kidney weight to body weight, compared with wild-type littermates

• at 3-4 months, homozygotes displayed no gross morphological defects in coronary, carotid or aortic sections

• also, homozygous mutant mice displayed normal aldosterone levels relative to wild-type

aortic hypertrophy ( J:86774 )

• medial areas of aortic sections from homozygous mutant mice were significantly larger than those of wild-type littermates

abnormal kidney vasculature morphology ( J:81893 )

• homozygous mutant mice displayed renovascular defects including medial thickening of renal arterioles, indicating vascular smooth muscle cell hypertrophy and/or hyperproliferation; however, there was no evidence of cardiac hypertrophy in these same animals

increased systemic arterial blood pressure ( J:81893 , J:86774 )

• anesthetized homozygous mutant mice were strongly hypertensive: their mean aortic blood pressure was 135 3 mmHg, compared with 84 6 mmHg for isogenic wild-type control mice; hypertension was confirmed in unanesthetized freely moving mice (J:81893)

• transthoracic echocardiography of 6-month-old homozygous mutant mice revealed no significant reduction in systolic contractile function or evidence of hypertrophy relative to wild-type (J:81893)

• homozygous mutant mice displayed small increases in blood pressure in response to a maximal dose of angiotensin II or phenylephrine, thus eliminating hypertrophy of the resistance vasculature as the cause of the hypertensive phenotype (J:81893)

• homozygous mutant mice displayed significantly prolonged vasoconstrictor responses of the peripheral resistance vasculature in vivo and of aortic vascular smooth muscle cells in vitro; by prolonging the rate at which vasoconstrictor signaling terminates, the mutation is proposed to increase the duration of contraction by the resistance vasculature, thus elevating blood pressure (J:81893)

• in support of this hypothesis, the mutant hypertensive phenotype was reversed within minutes following either blockade of angiotensin II production with an ACE inhibitor or antagonism of AT1 receptors; also, the rate of blood pressure decline in homozygous mutant mice infused with an AT1 antagonist was slower than that in similarly treated wild-type littermates (J:81893)

• hypertension was confirmed in conscious, freely moving homozygous mutant mice (J:86774)

abnormal blood vessel physiology ( J:86774 )

• vascular ring studies revealed increased vascular contraction in response to Gq-coupled receptor agonists and significantly attenuated vascular relaxation in response to cGMP in endothelium-intact aortic rings from homozygous mutant mice

hematopoietic system phenotype ( J:77273 )

N	• original characterization of homozygous mutant mice demonstrated that these mice are viable, fertile, and normal with respect to growth, anatomy, and differentiation of all hematopoietic lineages (including neutrophils, macrophages, erythrocytes, and platelets)

abnormal T cell proliferation ( J:77273 )

• in vitro, T cells from homozygous mutant mice exhibited a reduction in proliferation and IL-2 production; in contrast, B cell activation appeared unaffected, relative to wild-type

• moreover, homozygous mutant mice developed a significantly decreased and delayed footpad swelling reaction, indicating an impaired antiviral response in vivo

abnormal T cell proliferation ( J:77273 )

• in vitro, T cells from homozygous mutant mice exhibited a reduction in proliferation and IL-2 production; in contrast, B cell activation appeared unaffected, relative to wild-type

• moreover, homozygous mutant mice developed a significantly decreased and delayed footpad swelling reaction, indicating an impaired antiviral response in vivo

abnormal kidney vasculature morphology ( J:81893 )

• homozygous mutant mice displayed renovascular defects including medial thickening of renal arterioles, indicating vascular smooth muscle cell hypertrophy and/or hyperproliferation; however, there was no evidence of cardiac hypertrophy in these same animals

nervous system phenotype ( J:77273 )

N	• morphological studies revealed that the number of neurons in the hippocampus, in other brain nuclei, the brainstem, cerebellum, and cortex were unaffected

abnormal hippocampus CA1 region morphology ( J:77273 )

• hippocampal CA1 neurons of mutant mice showed a significant decrease in the density of apical and basilar spines compared with those of control littermates

abnormal nervous system electrophysiology ( J:77273 )

• the morphological deficit in spine numbers of mutant CA1 neurons correlated with a significantly reduced electrical input/output relationship, indicating both impaired synaptic development and basal electrical activity of hippocampal CA1 neurons

abnormal T cell proliferation ( J:77273 )

• in vitro, T cells from homozygous mutant mice exhibited a reduction in proliferation and IL-2 production; in contrast, B cell activation appeared unaffected, relative to wild-type

• moreover, homozygous mutant mice developed a significantly decreased and delayed footpad swelling reaction, indicating an impaired antiviral response in vivo

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

Contributing Projects: Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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