Structure and function of the Arp2/3 complex

Rd, Mullins; Td, Pollard

doi:10.1016/s0959-440x(99)80034-7

Cited by 126 publications

(46 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The first mechanism is mediated by the Arp2/3 complex (Goley and Welch, 2006;Mullins and Pollard, 1999;Welch et al, 1997;Welch and Mullins, 2002) that interacts with the surface of the existing actin filaments to create sites of branching for new actin polymerization and ensure actin assembly into the dendritic network that drives the protrusion of lamellipodia. The second mechanism is mediated by formins (Goode and Eck, 2007;Pruyne et al, 2002;Zigmond, 2004;Zigmond et al, 1998) that drive actin assembly into parallel cross-linked bundles that serve as a structural basis for filopodia.…”

Section: Basic Principles Of Cell Migration Overall Structure Of the mentioning

confidence: 99%

Cell biology of embryonic migration

Kurosaka¹,

Kashina²

2008

Birth Defects Research Pt C

117

View full text Add to dashboard Cite

Cell migration is an evolutionarily conserved mechanism that underlies the development and functioning of uni-and multicellular organisms and takes place in normal and pathogenic processes, including various events of embryogenesis, wound healing, immune response, cancer metastases, and angiogenesis. Despite the differences in the cell types that take part in different migratory events, it is believed that all of these migrations occur by similar molecular mechanisms, whose major components have been functionally conserved in evolution and whose perturbation leads to severe developmental defects. These mechanisms involve intricate cytoskeleton-based molecular machines that can sense the environment, respond to signals, and modulate the entire cell behavior. A big question that has concerned the researchers for decades relates to the coordination of cell migration in situ and its relation to the intracellular aspects of the cell migratory mechanisms. Traditionally, this question has been addressed by researchers that considered the intra-and extracellular mechanisms driving migration in separate sets of studies. As more data accumulate researchers are now able to integrate all of the available information and consider the intracellular mechanisms of cell migration in the context of the developing organisms that contain additional levels of complexity provided by extracellular regulation. This review provides a broad summary of the existing and emerging data in the cell and developmental biology fields regarding cell migration during development.

show abstract

Section: Basic Principles Of Cell Migration Overall Structure Of the mentioning

confidence: 99%

Cell biology of embryonic migration

Kurosaka¹,

Kashina²

2008

Birth Defects Research Pt C

117

View full text Add to dashboard Cite

show abstract

“…The cytoskeleton in lamellipodia is organized as a dense, branching actin network. This organization of actin is mediated, in part, by the Arp2/3 complex, which regulates actin nucleation (Mullins and Pollard, 1999;Svitkina and Borisy, 1999;Welch, 1999).…”

Section: R-ras Regulates the Establishment Of Cellular Polaritymentioning

confidence: 99%

R-Ras Controls Membrane Protrusion and Cell Migration through the Spatial Regulation of Rac and Rho

Wozniak

Kwong

Chodniewicz

et al. 2005

MBoC

View full text Add to dashboard Cite

Although it is known that the spatial coordination of Rac and Rho activity is essential for cell migration, the molecular mechanisms regulating these GTPases during migration are unknown. We found that the expression of constitutively activated R-Ras (38V) blocked membrane protrusion and random migration. In contrast, expression of dominant negative R-Ras (41A) enhanced migrational persistence and membrane protrusion. Endogenous R-Ras is necessary for cell migration, as cells that were transfected with siRNA for R-Ras did not migrate. Expression of R-Ras (38V) decreased Rac activity and increased Rho activity around the entire cell periphery, whereas expression of dominant negative R-Ras (41A) showed the converse, suggesting that R-Ras can spatially activate Rho and inactivate Rac. Consistent with this role, endogenous R-Ras localized and was preferentially activated at the leading edge of migratory cells in response to adhesion. The effects of R-Ras on cell migration are mediated by PI3-Kinase, as an effector mutant that uncouples PI3-Kinase binding from R-Ras (38V) rescued migration. From these data, we hypothesize that R-Ras plays a key role in cell migration by locally regulating the switch from Rac to Rho activity after membrane protrusion and adhesion.

show abstract

“…The organization and dynamics of F-actin are tightly controlled by an array of regulatory proteins, including the actin related protein 2/3 (ARP2/3) complex and its activator, the SCAR/WAVE complex (called SCAR here for simplicity), which facilitate nucleation of new short F-actin branches from existing filaments (Machesky and Insall, 1998;Mullins and Pollard, 1999). All components of the ARP2/3-SCAR complex are present in Arabidopsis thaliana (Deeks and Hussey, 2005;Szymanski, 2005), and through mutant analyses, this complex has recently been implicated in the control of root elongation (Dyachok et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

SCAR Mediates Light-Induced Root Elongation inArabidopsisthrough Photoreceptors and Proteasomes

et al. 2011

View full text Add to dashboard Cite

The ARP2/3 complex, a highly conserved nucleator of F-actin, and its activator, the SCAR complex, are essential for growth in plants and animals. In this article, we present a pathway through which roots of Arabidopsis thaliana directly perceive light to promote their elongation. The ARP2/3-SCAR complex and the maintenance of longitudinally aligned F-actin arrays are crucial components of this pathway. The involvement of the ARP2/3-SCAR complex in light-regulated root growth is supported by our finding that mutants of the SCAR complex subunit BRK1/HSPC300, or other individual subunits of the ARP2/3-SCAR complex, showed a dramatic inhibition of root elongation in the light, which mirrored reduced growth of wild-type roots in the dark. SCAR1 degradation in dark-grown wild-type roots by constitutive photomorphogenic 1 (COP1) E3 ligase and 26S proteasome accompanied the loss of longitudinal F-actin and reduced root growth. Light perceived by the root photoreceptors, cryptochrome and phytochrome, suppressed COP1-mediated SCAR1 degradation. Taken together, our data provide a biochemical explanation for light-induced promotion of root elongation by the ARP2/3-SCAR complex.

show abstract

Structure and function of the Arp2/3 complex

Cited by 126 publications

References 15 publications

Cell biology of embryonic migration

Cell biology of embryonic migration

R-Ras Controls Membrane Protrusion and Cell Migration through the Spatial Regulation of Rac and Rho

SCAR Mediates Light-Induced Root Elongation inArabidopsisthrough Photoreceptors and Proteasomes

Contact Info

Product

Resources

About