Possible role of the receptor protein tyrosine phosphatase HmLAR2 in interbranch repulsion in a leech embryonic cell

Baker, Maureen; Rauth, Sarah J.; Macagno, Eduardo R.

doi:10.1002/1097-4695(200010)45:1<47::aid-neu5>3.0.co;2-c

Cited by 30 publications

(17 citation statements)

References 42 publications

(55 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Perturbation of the leech LAR homolog (HmLAR2) results in abnormal neuronal projections (Gershon et al, 1998). Recent studies suggest that HmLAR2 may regulate mutual repulsion via a homophilic binding mechanism (Baker and Macagno, 2000a, b;Baker et al, 2000). The regulation of tyrosine phosphorylation by RPTPs may affect neurite outgrowth by "steering" growth cones along the appropriate pathway to establish a spatiotemporal pattern of neuronal connections, via both permissive and repulsive responses.…”

Section: Discussionmentioning

confidence: 99%

Rho GTPases regulate PTPμ-mediated nasal neurite outgrowth and temporal repulsion of retinal ganglion cell neurons

Major

Brady‐Kalnay

2007

Molecular and Cellular Neuroscience

View full text Add to dashboard Cite

Members of the receptor protein tyrosine phosphatase (RPTP) subfamily of cell adhesion molecules (CAMs) mediate neurite outgrowth and growth cone repulsion. PTPmu is a growth permissive substrate for nasal retinal ganglion cell (RGC) neurites and a growth inhibitory substrate for temporal RGCs. In this manuscript, we demonstrate that the distinct PTPmu-dependent phenotypes of nasal outgrowth and temporal repulsion are regulated by Rho GTPases. The role of Rho GTPases in the regulation of nasal outgrowth and temporal repulsion was tested by utilizing dominant negative and constitutively active forms of Rac1, RhoA and Cdc42 in Bonhoeffer stripe assays. Nasal neurite outgrowth on PTPmu was blocked by Cdc42-DN. Temporal repulsion to a PTPmu substrate was substantially reduced by addition of Cdc42-DN. The molecule that regulates the switch between permissive versus repulsive responses to PTPmu is Rac1 for temporal neurons. Inhibition of Rac1 is required for repulsion of temporal neurons. Interestingly, adding Rac1-CA to temporal RGC neurons converted PTPmu-dependent repulsion to a permissive response. In addition, adding exogenous Rac1-DN to nasal neurons induced a phenotype switch from a permissive to repulsive response to PTPmu. Together these data suggest that Cdc42 activity is required for both permissive and repulsive responses to PTPmu. However, the key to PTPmu-dependent repulsion is inhibition of Rac1 activity in temporal RGC neurons.

show abstract

Section: Discussionmentioning

confidence: 99%

Rho GTPases regulate PTPμ-mediated nasal neurite outgrowth and temporal repulsion of retinal ganglion cell neurons

Major

Brady‐Kalnay

2007

Molecular and Cellular Neuroscience

View full text Add to dashboard Cite

show abstract

“…AntiGFP immunocytochemistry was performed on wholemount embryos using anti-GFP mAb 3E6 and an Alexa 488 conjugated goat anti-mouse IgG (both from Molecular Probes) using established methods (Baker et al, 2000).…”

Section: In Situ Hybridizations and Immunocytochemistry On Whole-mounmentioning

confidence: 99%

“…Baptista et al, 1990;Blair et al, 1990;Gan and Macagno, 1995;Becker et al, 1996;Lans et al, 1996;Johnson et al, 2000;Jellies et al, 2000). Moreover, using fluorescent probes, the leech's large and accessible neurons can be observed down to the level of the growth cone filopodia, in situ and across time, in the intact, living embryo (Wang and Macagno, 1997;Baker et al, 2000Baker et al, , 2003.…”

Section: Introductionmentioning

confidence: 99%

Characterizations of Hirudo medicinalis DNA promoters for targeted gene expression

Baker

Macagno

2006

Journal of Neuroscience Methods

Self Cite

View full text Add to dashboard Cite

“…2). A related leech RPTP, HmLAR2, appears to act through homophilic interactions as well (9). Although homophilic ligands exist, no physiological signi cance has been de nitively demonstrated for these binding interactions.…”

Section: Are Rptps Really Receptors?mentioning

confidence: 99%

Ligands and Signaling Through Receptor‐Type Tyrosine Phosphatases

Bixby¹

2001

IUBMB Life

View full text Add to dashboard Cite

SummaryVirtually every aspect of cellular proliferation and differentiation is regulated by changes in tyrosine phosphorylation. Tyrosine phosphorylation, in turn, is controlled by the opposing activities of protein tyrosine kinases (PTKs) and protein tyrosine phosphatases (PTPs). PTKs are often transmembrane proteins (receptor PTKs) whose enzymatic activities and signaling functions are tightly regulated by the binding of speci c ligands. A variety of transmembrane PTPs has also been identi ed; these proteins are called receptor PTPs (RPTPs), but in most cases their roles as receptors are very poorly understood. This review discusses the evidence that RPTPs are actually receptors for extrinsic ligands, and the extent to which interactions with putative ligands are known or suspected to cause changes in enzymatic activity. Finally, some of the RPTP substrates believed to be physiologically important are described. The evidence gathered to date suggests that models derived from studies of receptor PTKs may be too simple to account for the diversity and complexity of mechanisms through which ligand binding controls RPTP function.

show abstract

Possible role of the receptor protein tyrosine phosphatase HmLAR2 in interbranch repulsion in a leech embryonic cell

Cited by 30 publications

References 42 publications

Rho GTPases regulate PTPμ-mediated nasal neurite outgrowth and temporal repulsion of retinal ganglion cell neurons

Rho GTPases regulate PTPμ-mediated nasal neurite outgrowth and temporal repulsion of retinal ganglion cell neurons

Characterizations of Hirudo medicinalis DNA promoters for targeted gene expression

Ligands and Signaling Through Receptor‐Type Tyrosine Phosphatases

Contact Info

Product

Resources

About