Negative cooperativity regulates ligand activation of DIAPH1 and other diaphanous related formins

Abstract DIAPH1 is a member of the family of Diaphanous Related Formins (DRFs) implicated in cell migration and cytokinesis. DRFs are maintained in an autoinhibited state by the intramolecular association between diaphanous inhibitory (DID) and diaphanous autoregulatory (DAD) domains. Actin polymeri...

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Main Authors: G. G. Theophall, A. Premo, S. Reverdatto, E. Omojowolo, P. Nazarian, D. S. Burz, R. Ramasamy, A. M. Schmidt, A. Shekhtman
Format: Article
Language:English
Published: Nature Portfolio 2025-05-01
Series:Communications Biology
Online Access:https://doi.org/10.1038/s42003-025-08222-5
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author G. G. Theophall
A. Premo
S. Reverdatto
E. Omojowolo
P. Nazarian
D. S. Burz
R. Ramasamy
A. M. Schmidt
A. Shekhtman
author_facet G. G. Theophall
A. Premo
S. Reverdatto
E. Omojowolo
P. Nazarian
D. S. Burz
R. Ramasamy
A. M. Schmidt
A. Shekhtman
author_sort G. G. Theophall
collection DOAJ
description Abstract DIAPH1 is a member of the family of Diaphanous Related Formins (DRFs) implicated in cell migration and cytokinesis. DRFs are maintained in an autoinhibited state by the intramolecular association between diaphanous inhibitory (DID) and diaphanous autoregulatory (DAD) domains. Actin polymerization requires the binding of activated RhoA to the GTPase binding domain (GBD) of DIAPH1 and the dissociation of DAD. In the presence of excess RhoA, actin polymerization is only partially activated. Using monomeric domain constructs of DIAPH1, the sequential binding affinities of RhoA and DAD to GBD-DID were characterized. Binding of RhoA and DAD were negatively cooperative requiring a 100-fold greater concentration of DAD to achieve saturation when RhoA binding site was occupied. The unimolecular architecture of full length DIAPH1 establishes an effective concentration of DAD in the micromolar range, which is 100-fold larger than the intrinsic affinity of DAD for DID. The effective concentration is large enough to maintain DIAPH1 autoinhibition, yet small enough to permit partial activation of DIAPH1 after RhoA binding. By exploiting negative cooperativity, DIAPH1 maintains a reserve of inactivated molecules enabling gradual responses to cellular processes that require prolonged and sustained regulation. The proposed mechanism is extended to other DIAPH1 activating ligands and broadly applicable to all DRFs.
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spelling doaj-art-db60fbc64fe34407bbff5f451cb645aa2025-08-20T01:53:19ZengNature PortfolioCommunications Biology2399-36422025-05-018111210.1038/s42003-025-08222-5Negative cooperativity regulates ligand activation of DIAPH1 and other diaphanous related forminsG. G. Theophall0A. Premo1S. Reverdatto2E. Omojowolo3P. Nazarian4D. S. Burz5R. Ramasamy6A. M. Schmidt7A. Shekhtman8Department of Chemistry, State University of New York at AlbanyDepartment of Chemistry, State University of New York at AlbanyDepartment of Chemistry, State University of New York at AlbanyDepartment of Chemistry, State University of New York at AlbanyDepartment of Chemistry, State University of New York at AlbanyDepartment of Chemistry, State University of New York at AlbanyDiabetes Research Program, Department of Medicine, New York University Grossman School of MedicineDiabetes Research Program, Department of Medicine, New York University Grossman School of MedicineDepartment of Chemistry, State University of New York at AlbanyAbstract DIAPH1 is a member of the family of Diaphanous Related Formins (DRFs) implicated in cell migration and cytokinesis. DRFs are maintained in an autoinhibited state by the intramolecular association between diaphanous inhibitory (DID) and diaphanous autoregulatory (DAD) domains. Actin polymerization requires the binding of activated RhoA to the GTPase binding domain (GBD) of DIAPH1 and the dissociation of DAD. In the presence of excess RhoA, actin polymerization is only partially activated. Using monomeric domain constructs of DIAPH1, the sequential binding affinities of RhoA and DAD to GBD-DID were characterized. Binding of RhoA and DAD were negatively cooperative requiring a 100-fold greater concentration of DAD to achieve saturation when RhoA binding site was occupied. The unimolecular architecture of full length DIAPH1 establishes an effective concentration of DAD in the micromolar range, which is 100-fold larger than the intrinsic affinity of DAD for DID. The effective concentration is large enough to maintain DIAPH1 autoinhibition, yet small enough to permit partial activation of DIAPH1 after RhoA binding. By exploiting negative cooperativity, DIAPH1 maintains a reserve of inactivated molecules enabling gradual responses to cellular processes that require prolonged and sustained regulation. The proposed mechanism is extended to other DIAPH1 activating ligands and broadly applicable to all DRFs.https://doi.org/10.1038/s42003-025-08222-5
spellingShingle G. G. Theophall
A. Premo
S. Reverdatto
E. Omojowolo
P. Nazarian
D. S. Burz
R. Ramasamy
A. M. Schmidt
A. Shekhtman
Negative cooperativity regulates ligand activation of DIAPH1 and other diaphanous related formins
Communications Biology
title Negative cooperativity regulates ligand activation of DIAPH1 and other diaphanous related formins
title_full Negative cooperativity regulates ligand activation of DIAPH1 and other diaphanous related formins
title_fullStr Negative cooperativity regulates ligand activation of DIAPH1 and other diaphanous related formins
title_full_unstemmed Negative cooperativity regulates ligand activation of DIAPH1 and other diaphanous related formins
title_short Negative cooperativity regulates ligand activation of DIAPH1 and other diaphanous related formins
title_sort negative cooperativity regulates ligand activation of diaph1 and other diaphanous related formins
url https://doi.org/10.1038/s42003-025-08222-5
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