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Altered rhodopsin accessibility in the retinal dystrophic mouse.
Biochemical and Biophysical Research Communications
|October 30, 1985
Summary
In 7-day-old rd mouse retinas, rhodopsin quantity is unchanged but its accessibility to antirhodopsin antibodies is reduced, particularly at the carboxyl terminus.
Area of Science:
- Retinal degeneration research
- Molecular biology of vision
- Photoreceptor protein analysis
Background:
- Retinitis pigmentosa (RP) is a group of inherited retinal diseases.
- The rd mouse is a common model for studying human RP.
- Rhodopsin is the primary light-sensory protein in rod photoreceptors.
Purpose of the Study:
- To investigate alterations in rhodopsin in the rd mouse retina.
- To determine if rhodopsin quantity or accessibility is affected in rd mice.
- To identify potential regions of rhodopsin affected by the rd mutation.
Main Methods:
- Immunohistochemical analysis of retinas from 7-day-old rd and normal mice using antirhodopsin antisera.
- Western blot analysis of denatured rhodopsin from rd and normal retinas.
- Use of antisera against synthetic peptides corresponding to the rhodopsin carboxyl terminus.
Main Results:
- Retinas from 7-day-old rd mice showed reduced reactivity with antirhodopsin antisera compared to normal retinas.
- Antisera targeting the rhodopsin carboxyl terminus also exhibited decreased reactivity with rd retinas.
- Western blots revealed no significant difference in the total quantity of rhodopsin between rd and normal retinas.
Conclusions:
- In 7-day-old rd mouse retinas, rhodopsin quantity remains stable.
- The rd mutation leads to decreased accessibility of rhodopsin to antibodies, suggesting conformational changes.
- Altered accessibility is likely located at the carboxyl terminus of rhodopsin.