Holger Knaut
· Associate ProfessorVerifiedNew York University · Cell Biology
Active 1996–2025
About
Holger Knaut, PhD, is an Associate Professor in the Department of Cell Biology at NYU Grossman School of Medicine. His research focuses on embryonic development involving extensive cell and tissue movements, particularly how cells interpret guidance cues and interact with tissues during migration to reach their final destinations and assemble into organs. He combines in vivo imaging with embryological and genetic manipulations, utilizing zebrafish as a model organism, to study cell migration processes. His work addresses two main models: the assembly of the trigeminal sensory ganglion, where he investigates how disperse neuronal precursors migrate and assemble into a functional unit, and muscle precursor migration, where he studies how related cells migrate to different targets and attach to specific sites on the skeleton. His research aims to understand the molecular mechanisms guiding these migrations, which can contribute to knowledge about organ formation and potential developmental disorders. Knaut's contributions advance understanding of how migrating cells of different types coordinate with tissues to form complex structures and functional networks in embryonic development.
Research topics
- Cell biology
- Biology
- Chemistry
- Genetics
- Biophysics
- Neuroscience
- Anatomy
- Biochemistry
- Computational biology
Selected publications
Cold Spring Harbor Perspectives in Biology · 2025-09-22 · 1 citations
articleOpen accessSenior authorfor most sensitive signaling, mechanical coupling among cells for averaging directional sensing in a tissue, and large rear traction stresses to propel the tissue forward. Many of these strategies likely apply to collectively migrating cells in other contexts and should thus provide insights with direct relevance to human health.
RhoA GEF Mcf2lb regulates rosette integrity during collective cell migration
Development · 2024-01-01 · 6 citations
articleOpen accessMulticellular rosettes are transient epithelial structures that serve as important cellular intermediates in the formation of diverse organs. Using the zebrafish posterior lateral line primordium (pLLP) as a model system, we investigated the role of the RhoA GEF Mcf2lb in rosette morphogenesis. The pLLP is a group of ∼150 cells that migrates along the zebrafish trunk and is organized into epithelial rosettes; these are deposited along the trunk and will differentiate into sensory organs called neuromasts (NMs). Using single-cell RNA-sequencing and whole-mount in situ hybridization, we showed that mcf2lb is expressed in the pLLP during migration. Live imaging and subsequent 3D analysis of mcf2lb mutant pLLP cells showed disrupted apical constriction and subsequent rosette organization. This resulted in an excess number of deposited NMs along the trunk of the zebrafish. Cell polarity markers ZO-1 and Par-3 were apically localized, indicating that pLLP cells are properly polarized. In contrast, RhoA activity, as well as signaling components downstream of RhoA, Rock2a and non-muscle Myosin II, were diminished apically. Thus, Mcf2lb-dependent RhoA activation maintains the integrity of epithelial rosettes.
Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · 2023-06-01
dataset1st authorCorrespondingZenodo (CERN European Organization for Nuclear Research) · 2023-11-17
datasetOpen accessSenior authorIn animals, cells often move as collectives to shape organs, close wounds, or—in the case of disease—metastasize. To accomplish this, cells need to generate force to propel themselves forward. The motility of singly migrating cells is driven largely by an interplay between Rho GTPase signaling and the actin network. Whether cells migrating as collectives use the same machinery for motility is unclear. Using the zebrafish posterior lateral line primordium as a model for collective cell migration, we find that active RhoA and myosin II cluster on the basal sides of the primordium cells and are required for primordium motility. Positive and negative feedbacks cause RhoA and myosin II activities to pulse. These pulses of RhoA signaling stimulate actin polymerization at the tip of the protrusions and myosin II-dependent actin flow and protrusion retraction at the base of the protrusions, and deform the basement membrane underneath the migrating primordium. This suggests that RhoA-induced actin flow on the basal sides of the cells constitutes the motor that pulls the primordium forward, a scenario that likely underlies collective migration in other—but not all—contexts.
bioRxiv (Cold Spring Harbor Laboratory) · 2023-10-05 · 1 citations
preprintOpen accessSenior authorCorrespondingIn animals, cells often move as collectives to shape organs, close wounds, or-in the case of disease-metastasize. To accomplish this, cells need to generate force to propel themselves forward. The motility of singly migrating cells is driven largely by an interplay between Rho GTPase signaling and the actin network (Yamada and Sixt, 2019). Whether cells migrating as collectives use the same machinery for motility is unclear. Using the zebrafish posterior lateral line primordium as a model for collective cell migration, we find that active RhoA and myosin II cluster on the basal sides of the primordium cells and are required for primordium motility. Positive and negative feedbacks cause RhoA and myosin II activities to pulse. These pulses of RhoA signaling stimulate actin polymerization at the tip of the protrusions and myosin II-dependent actin flow and protrusion retraction at the base of the protrusions, and deform the basement membrane underneath the migrating primordium. This suggests that RhoA-induced actin flow on the basal sides of the cells constitutes the motor that pulls the primordium forward, a scenario that likely underlies collective migration in other-but not all (Bastock and Strutt, 2007; Lebreton and Casanova, 2013; Matthews et al., 2008)-contexts.
Zenodo (CERN European Organization for Nuclear Research) · 2023-11-17
datasetOpen accessSenior authorIn animals, cells often move as collectives to shape organs, close wounds, or—in the case of disease—metastasize. To accomplish this, cells need to generate force to propel themselves forward. The motility of singly migrating cells is driven largely by an interplay between Rho GTPase signaling and the actin network. Whether cells migrating as collectives use the same machinery for motility is unclear. Using the zebrafish posterior lateral line primordium as a model for collective cell migration, we find that active RhoA and myosin II cluster on the basal sides of the primordium cells and are required for primordium motility. Positive and negative feedbacks cause RhoA and myosin II activities to pulse. These pulses of RhoA signaling stimulate actin polymerization at the tip of the protrusions and myosin II-dependent actin flow and protrusion retraction at the base of the protrusions, and deform the basement membrane underneath the migrating primordium. This suggests that RhoA-induced actin flow on the basal sides of the cells constitutes the motor that pulls the primordium forward, a scenario that likely underlies collective migration in other—but not all—contexts.
Current Biology · 2023-12-13 · 18 citations
articleOpen accessSenior authorCorrespondingFocal adhesion-mediated cell anchoring and migration: from<i>in vitro</i>to<i>in vivo</i>
Development · 2022-05-15 · 70 citations
articleOpen accessSenior authorCell-extracellular matrix interactions have been studied extensively using cells cultured in vitro. These studies indicate that focal adhesion (FA)-based cell-extracellular matrix interactions are essential for cell anchoring and cell migration. Whether FAs play a similarly important role in vivo is less clear. Here, we summarize the formation and function of FAs in cultured cells and review how FAs transmit and sense force in vitro. Using examples from animal studies, we also describe the role of FAs in cell anchoring during morphogenetic movements and cell migration in vivo. Finally, we conclude by discussing similarities and differences in how FAs function in vitro and in vivo.
Faculty Opinions recommendation of Cell division in tissues enables macrophage infiltration.
Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · 2022-07-04
dataset1st authorCorrespondingFaculty Opinions – Post-Publication Peer Review of the Biomedical Literature · 2022-11-09
dataset1st authorCorresponding
Recent grants
Molecular and Cellular Control of Collective Cell Migration.
NIH · $2.4M · 2018–2024
Transposon-mediated BAC Transgenesis
NIH · $249k · 2013–2015
Molecular and Cellular Regulation of Fgf signaling
NIH · $466k · 2018–2021
Molecular regulation of trigeminal sensory ganglia development
NIH · $2.2M · 2011–2018
Engineering tools for rapid loss of protein function in model organisms
NIH · $466k · 2016–2019
Frequent coauthors
- 26 shared
Naoya Yamaguchi
University of Cambridge
- 16 shared
Matthew G. Ryan
Leeds Teaching Hospitals NHS Trust
- 16 shared
Russ Hille
University of California, Riverside
- 16 shared
Jong Hwa Kim
Korea Basic Science Institute
- 13 shared
Tugba Colak-Champollion
New York University
- 11 shared
Michael Cammer
New York University
- 11 shared
Weiyi Qian
New York University
- 7 shared
Christiane Nüsslein–Volhard
Max Planck Institute for Biology
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