Abstract：
:Mice carrying the rd mutation are affected with an autosomal recessive disease characterized by the total degeneration of retinal photoreceptor cells, which begins at postnatal day 8 and reaches completion by 3 wk of life. Biochemical studies have led to the proposal that a lesion in cGMP metabolism may be the cause of the rd photoreceptor degeneration, since cGMP reaches abnormally high levels in the rd retina a few days before the morphological pathology starts. The abnormal cGMP level is due to deficient cGMP-phosphodiesterase (cGMP-PDE) activity. A cDNA for the gamma-subunit of mouse cGMP-PDE has recently been cloned and characterized. We have mapped this cDNA to mouse chromosome 11 using a panel comprised of 19 hamster-mouse somatic cell hybrids by Southern blot hybridization. Our results suggest that the structural gene for the gamma-subunit of cGMP-PDE from mouse retina, which we have designated 'Pdeg', is not the primary defect in rd disease, as the locus of this genetic defect is on mouse chromosome 5.
journal_name
Exp Eye Resjournal_title
Experimental eye researchauthors
Danciger M,Tuteja N,Kozak CA,Farber DBdoi
10.1016/s0014-4835(89)80079-xsubject
Has Abstractpub_date
1989-02-01 00:00:00pages
303-8issue
2eissn
0014-4835issn
1096-0007journal_volume
48pub_type
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pub_type： 更正并重新发布的文章,杂志文章
doi：
更新日期：2004-12-01 00:00:00
