Lifetime of major histocompatibility complex class-I membrane clusters is controlled by the actin cytoskeleton

Yael Lavi, Nir Gov, Michael A Edidin, Levi A. Gheber

Research output: Contribution to journalArticle

Abstract

Lateral heterogeneity of cell membranes has been demonstrated in numerous studies showing anomalous diffusion of membrane proteins; it has been explained by models and experiments suggesting dynamic barriers to free diffusion, that temporarily confine membrane proteins into microscopic patches. This picture, however, comes short of explaining a steady-state patchy distribution of proteins, in face of the transient opening of the barriers. In our previous work we directly imaged persistent clusters of MHC-I, a type I transmembrane protein, and proposed a model of a dynamic equilibrium between proteins newly delivered to the cell surface by vesicle traffic, temporary confinement by dynamic barriers to lateral diffusion, and dispersion of the clusters by diffusion over the dynamic barriers. Our model predicted that the clusters are dynamic, appearing when an exocytic vesicle fuses with the plasma membrane and dispersing with a typical lifetime that depends on lateral diffusion and the dynamics of barriers. In a subsequent work, we showed this to be the case. Here we test another prediction of the model, and show that changing the stability of actin barriers to lateral diffusion changes cluster lifetimes. We also develop a model for the distribution of cluster lifetimes, consistent with the function of barriers to lateral diffusion in maintaining MHC-I clusters.

Original languageEnglish (US)
Pages (from-to)1543-1550
Number of pages8
JournalBiophysical Journal
Volume102
Issue number7
DOIs
StatePublished - Apr 4 2012

Fingerprint

Major Histocompatibility Complex
Actin Cytoskeleton
Membranes
Membrane Proteins
Cell Membrane
Proteins
Actins

ASJC Scopus subject areas

  • Biophysics

Cite this

Lifetime of major histocompatibility complex class-I membrane clusters is controlled by the actin cytoskeleton. / Lavi, Yael; Gov, Nir; Edidin, Michael A; Gheber, Levi A.

In: Biophysical Journal, Vol. 102, No. 7, 04.04.2012, p. 1543-1550.

Research output: Contribution to journalArticle

@article{7dc449e6522e4a36946ca3d97958b85b,
title = "Lifetime of major histocompatibility complex class-I membrane clusters is controlled by the actin cytoskeleton",
abstract = "Lateral heterogeneity of cell membranes has been demonstrated in numerous studies showing anomalous diffusion of membrane proteins; it has been explained by models and experiments suggesting dynamic barriers to free diffusion, that temporarily confine membrane proteins into microscopic patches. This picture, however, comes short of explaining a steady-state patchy distribution of proteins, in face of the transient opening of the barriers. In our previous work we directly imaged persistent clusters of MHC-I, a type I transmembrane protein, and proposed a model of a dynamic equilibrium between proteins newly delivered to the cell surface by vesicle traffic, temporary confinement by dynamic barriers to lateral diffusion, and dispersion of the clusters by diffusion over the dynamic barriers. Our model predicted that the clusters are dynamic, appearing when an exocytic vesicle fuses with the plasma membrane and dispersing with a typical lifetime that depends on lateral diffusion and the dynamics of barriers. In a subsequent work, we showed this to be the case. Here we test another prediction of the model, and show that changing the stability of actin barriers to lateral diffusion changes cluster lifetimes. We also develop a model for the distribution of cluster lifetimes, consistent with the function of barriers to lateral diffusion in maintaining MHC-I clusters.",
author = "Yael Lavi and Nir Gov and Edidin, {Michael A} and Gheber, {Levi A.}",
year = "2012",
month = "4",
day = "4",
doi = "10.1016/j.bpj.2012.01.042",
language = "English (US)",
volume = "102",
pages = "1543--1550",
journal = "Biophysical Journal",
issn = "0006-3495",
publisher = "Biophysical Society",
number = "7",

}

TY - JOUR

T1 - Lifetime of major histocompatibility complex class-I membrane clusters is controlled by the actin cytoskeleton

AU - Lavi, Yael

AU - Gov, Nir

AU - Edidin, Michael A

AU - Gheber, Levi A.

PY - 2012/4/4

Y1 - 2012/4/4

N2 - Lateral heterogeneity of cell membranes has been demonstrated in numerous studies showing anomalous diffusion of membrane proteins; it has been explained by models and experiments suggesting dynamic barriers to free diffusion, that temporarily confine membrane proteins into microscopic patches. This picture, however, comes short of explaining a steady-state patchy distribution of proteins, in face of the transient opening of the barriers. In our previous work we directly imaged persistent clusters of MHC-I, a type I transmembrane protein, and proposed a model of a dynamic equilibrium between proteins newly delivered to the cell surface by vesicle traffic, temporary confinement by dynamic barriers to lateral diffusion, and dispersion of the clusters by diffusion over the dynamic barriers. Our model predicted that the clusters are dynamic, appearing when an exocytic vesicle fuses with the plasma membrane and dispersing with a typical lifetime that depends on lateral diffusion and the dynamics of barriers. In a subsequent work, we showed this to be the case. Here we test another prediction of the model, and show that changing the stability of actin barriers to lateral diffusion changes cluster lifetimes. We also develop a model for the distribution of cluster lifetimes, consistent with the function of barriers to lateral diffusion in maintaining MHC-I clusters.

AB - Lateral heterogeneity of cell membranes has been demonstrated in numerous studies showing anomalous diffusion of membrane proteins; it has been explained by models and experiments suggesting dynamic barriers to free diffusion, that temporarily confine membrane proteins into microscopic patches. This picture, however, comes short of explaining a steady-state patchy distribution of proteins, in face of the transient opening of the barriers. In our previous work we directly imaged persistent clusters of MHC-I, a type I transmembrane protein, and proposed a model of a dynamic equilibrium between proteins newly delivered to the cell surface by vesicle traffic, temporary confinement by dynamic barriers to lateral diffusion, and dispersion of the clusters by diffusion over the dynamic barriers. Our model predicted that the clusters are dynamic, appearing when an exocytic vesicle fuses with the plasma membrane and dispersing with a typical lifetime that depends on lateral diffusion and the dynamics of barriers. In a subsequent work, we showed this to be the case. Here we test another prediction of the model, and show that changing the stability of actin barriers to lateral diffusion changes cluster lifetimes. We also develop a model for the distribution of cluster lifetimes, consistent with the function of barriers to lateral diffusion in maintaining MHC-I clusters.

UR - http://www.scopus.com/inward/record.url?scp=84859378549&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84859378549&partnerID=8YFLogxK

U2 - 10.1016/j.bpj.2012.01.042

DO - 10.1016/j.bpj.2012.01.042

M3 - Article

VL - 102

SP - 1543

EP - 1550

JO - Biophysical Journal

JF - Biophysical Journal

SN - 0006-3495

IS - 7

ER -