Photoreceptor pathology in the X-linked retinoschisis (XLRS) mouse results in delayed rod maturation and impaired light driven transducin translocation

Lucia Ziccardi, Camasamudram Vijayasarathy, Ronald A. Bush, Paul A. Sieving

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Light-activated movement of transducin-a (Gαt1) from rod photoreceptor outer segments (ROS) into inner segments (IS) enables rods to rapidly adapt to changes in light intensity. The threshold light intensity at which Gat1 translocates from ROS into IS is primarily determined by the rates of activation and inactivation of Gαt1. Loss- of- expression of the retina specific cell surface protein, retinoschsin (Rs1-KO), led to a dramatic 3–10 fold increase, depending on age, in the luminance threshold for transducin translocation from ROS into IS compared with wild-type control. In contrast, arrestin translocated from IS into ROS at the same light intensity both in WT and Rs1-KO mice. Biochemical changes, including reduced transducin protein levels and enhanced transducin GTPase activity, explain the shift in light intensity threshold for Gat1 translocation in Rs1-KO mice. These changes in Rs1-KO mice were also associated with age related alterations in photoreceptor morphology and transcription factor expression that suggest delayed photoreceptor maturation.

Original languageEnglish
Pages (from-to)559-566
Number of pages8
JournalAdvances in Experimental Medicine and Biology
Volume801
DOIs
Publication statusPublished - 2014

Fingerprint

Retinoschisis
Transducin
Pathology
Rod Cell Outer Segment
Retinal Rod Photoreceptor Cells
Light
Retinal Photoreceptor Cell Inner Segment
Arrestin
Retina
Luminance
Membrane Proteins
Transcription Factors
Chemical activation
Proteins

Keywords

  • Arrestin
  • Photoreceptors
  • Retinoschisis
  • Transducin
  • Translocation

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

Photoreceptor pathology in the X-linked retinoschisis (XLRS) mouse results in delayed rod maturation and impaired light driven transducin translocation. / Ziccardi, Lucia; Vijayasarathy, Camasamudram; Bush, Ronald A.; Sieving, Paul A.

In: Advances in Experimental Medicine and Biology, Vol. 801, 2014, p. 559-566.

Research output: Contribution to journalArticle

@article{dff8263729ad497e8d9c310798370141,
title = "Photoreceptor pathology in the X-linked retinoschisis (XLRS) mouse results in delayed rod maturation and impaired light driven transducin translocation",
abstract = "Light-activated movement of transducin-a (Gαt1) from rod photoreceptor outer segments (ROS) into inner segments (IS) enables rods to rapidly adapt to changes in light intensity. The threshold light intensity at which Gat1 translocates from ROS into IS is primarily determined by the rates of activation and inactivation of Gαt1. Loss- of- expression of the retina specific cell surface protein, retinoschsin (Rs1-KO), led to a dramatic 3–10 fold increase, depending on age, in the luminance threshold for transducin translocation from ROS into IS compared with wild-type control. In contrast, arrestin translocated from IS into ROS at the same light intensity both in WT and Rs1-KO mice. Biochemical changes, including reduced transducin protein levels and enhanced transducin GTPase activity, explain the shift in light intensity threshold for Gat1 translocation in Rs1-KO mice. These changes in Rs1-KO mice were also associated with age related alterations in photoreceptor morphology and transcription factor expression that suggest delayed photoreceptor maturation.",
keywords = "Arrestin, Photoreceptors, Retinoschisis, Transducin, Translocation",
author = "Lucia Ziccardi and Camasamudram Vijayasarathy and Bush, {Ronald A.} and Sieving, {Paul A.}",
year = "2014",
doi = "10.1007/978-1-4614-3209-8_71",
language = "English",
volume = "801",
pages = "559--566",
journal = "Advances in Experimental Medicine and Biology",
issn = "0065-2598",
publisher = "Springer New York",

}

TY - JOUR

T1 - Photoreceptor pathology in the X-linked retinoschisis (XLRS) mouse results in delayed rod maturation and impaired light driven transducin translocation

AU - Ziccardi, Lucia

AU - Vijayasarathy, Camasamudram

AU - Bush, Ronald A.

AU - Sieving, Paul A.

PY - 2014

Y1 - 2014

N2 - Light-activated movement of transducin-a (Gαt1) from rod photoreceptor outer segments (ROS) into inner segments (IS) enables rods to rapidly adapt to changes in light intensity. The threshold light intensity at which Gat1 translocates from ROS into IS is primarily determined by the rates of activation and inactivation of Gαt1. Loss- of- expression of the retina specific cell surface protein, retinoschsin (Rs1-KO), led to a dramatic 3–10 fold increase, depending on age, in the luminance threshold for transducin translocation from ROS into IS compared with wild-type control. In contrast, arrestin translocated from IS into ROS at the same light intensity both in WT and Rs1-KO mice. Biochemical changes, including reduced transducin protein levels and enhanced transducin GTPase activity, explain the shift in light intensity threshold for Gat1 translocation in Rs1-KO mice. These changes in Rs1-KO mice were also associated with age related alterations in photoreceptor morphology and transcription factor expression that suggest delayed photoreceptor maturation.

AB - Light-activated movement of transducin-a (Gαt1) from rod photoreceptor outer segments (ROS) into inner segments (IS) enables rods to rapidly adapt to changes in light intensity. The threshold light intensity at which Gat1 translocates from ROS into IS is primarily determined by the rates of activation and inactivation of Gαt1. Loss- of- expression of the retina specific cell surface protein, retinoschsin (Rs1-KO), led to a dramatic 3–10 fold increase, depending on age, in the luminance threshold for transducin translocation from ROS into IS compared with wild-type control. In contrast, arrestin translocated from IS into ROS at the same light intensity both in WT and Rs1-KO mice. Biochemical changes, including reduced transducin protein levels and enhanced transducin GTPase activity, explain the shift in light intensity threshold for Gat1 translocation in Rs1-KO mice. These changes in Rs1-KO mice were also associated with age related alterations in photoreceptor morphology and transcription factor expression that suggest delayed photoreceptor maturation.

KW - Arrestin

KW - Photoreceptors

KW - Retinoschisis

KW - Transducin

KW - Translocation

UR - http://www.scopus.com/inward/record.url?scp=84904786470&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84904786470&partnerID=8YFLogxK

U2 - 10.1007/978-1-4614-3209-8_71

DO - 10.1007/978-1-4614-3209-8_71

M3 - Article

C2 - 24664744

AN - SCOPUS:84904786470

VL - 801

SP - 559

EP - 566

JO - Advances in Experimental Medicine and Biology

JF - Advances in Experimental Medicine and Biology

SN - 0065-2598

ER -