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Titolo:
RGS9-1 is required for normal inactivation of mouse cone phototransduction
Autore:
Lyubarsky, A; Chen, CK; Naarendorp, F; Zhang, X; Wensel, T; Simon, M; Pugh, E;
Indirizzi:
Univ Penn, FM Kirby Ctr Mol Ophthalmol, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 phthalmol, Philadelphia, PA 19104 USA Univ Penn, Dept Ophthalmol, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 phthalmol, Philadelphia, PA 19104 USA Univ Utah, Dept Ophthalmol & Human Genet, Salt Lake City, UT USA Univ Utah Salt Lake City UT USA ol & Human Genet, Salt Lake City, UT USA Northeastern Univ, Dept Psychol, Boston, MA 02115 USA Northeastern Univ Boston MA USA 02115 Dept Psychol, Boston, MA 02115 USA Baylor Coll Med, Dept Biochem, Houston, TX 77030 USA Baylor Coll Med Houston TX USA 77030 Dept Biochem, Houston, TX 77030 USA CALTECH, Div Biol, Pasadena, CA 91125 USA CALTECH Pasadena CA USA 91125CALTECH, Div Biol, Pasadena, CA 91125 USA
Titolo Testata:
MOLECULAR VISION
fascicolo: 11, volume: 7, anno: 2001,
pagine: 71 - 78
SICI:
1090-0535(20010320)7:11<71:RIRFNI>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
GTPASE ACCELERATING PROTEIN; DRIVEN RETINAL RESPONSES; RHODOPSIN KINASE GENE; ROD PHOTORECEPTORS; SLOWED RECOVERY; MICE LACKING; BETA-SUBUNIT; A-WAVE; ELECTRORETINOGRAM; CYCLASE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Pugh, E Univ Penn, FM Kirby Ctr Mol Ophthalmol, Stellar Chance Bldg,Room 309B,422 Curie Blvd, Philadelphia, PA 19104 USA Univ Penn Stellar Chance Bldg,Room 309B,422 Curie Blvd Philadelphia PA USA 19104
Citazione:
A. Lyubarsky et al., "RGS9-1 is required for normal inactivation of mouse cone phototransduction", MOL VIS, 7(11), 2001, pp. 71-78

Abstract

PURPOSE: To test the hypothesis that Regulator of G-protein Signaling 9 (RGS9-1) is necessary for the normal inactivation of retinal cones. METHODS: Mice having the gene RGS9-1 inactivated in both alleles (RGS9-1 -/-) were tested between the ages 8-10 weeks with electroretinographic (ERG)protocols that isolate cone-driven responses. Immunohistochemistry was performed with a primary antibody against RGS9-1 (anti-RGS9-1c), with the secondary conjugated to fluorescein isothiocyanate, and with rhodamine-conjugated peanut agglutinin. RESULTS: (1) Immunohistochemistry showed RGS9-1 to be strongly expressed in the cones of wildtype (WT is C57BL/6) mice, but absent from the cones of RGS9-1 mice. (2) Cone-driven b-wave responses of dark-adapted RGS9-1 -/- mice had saturating amplitudes and sensitivities in the midwave and UV regions of the spectrum equal to or slightly greater than those of WT (C57BL/6) mice. (3) Cone-driven b-wave and a-wave responses of RGS9-1 -/- mice recovered much more slowly than those of WT after a strong conditioning flash: fora flash estimated to isomerize 1.2% of the M-cone pigment and 0.9% of the UV-cone pigment, recovery of 50% saturating amplitude was approximately 60-fold slower than in WT. CONCLUSIONS: (1) The amplitudes and sensitivities of the cone-driven responses indicate that cones and cone-driven neurons in RGS9-1 -/- mice have normal generator currents. (2) The greatly retarded recovery of cone-driven responses of RGS9-1 -/- mice relative to those of WT mice establishes that RGS9-1 is required for normal inactivation of the cone phototransduction cascades of both UV- and M-cones.

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Documento generato il 05/12/20 alle ore 14:08:17