Related Experiment Video
Updated: Aug 15, 2026

Optogenetic Inhibition of Rho1-Mediated Actomyosin Contractility Coupled with Measurement of Epithelial Tension in Drosophila Embryos
Published on: April 14, 2023
Src regulates the activity of the mammalian formin protein FHOD1
Sreenivas Koka1, Gerald T Minick, You Zhou
1Department of Dental Specialties, Mayo Clinic, Rochester, Minnesota, USA. koka.sreenivas@mayo.edu
Abstract:
The mammalian formin homology domain containing protein FHOD1 influences a variety of cellular events including cell migration, cytoskeletal arrangement, signal transduction, and gene expression. In this paper, we show that Src regulates a variety of FHOD1-associated effects. FHOD1 distribution to lamellipodia was prevented by the absence of Src. However, stress fiber formation induced by a C-terminal truncated form of FHOD1 was unaffected. Gene expression from an SRE-dependent promoter and from the skeletal actin promoter was induced by two truncated forms of FHOD1 and in both instances, inhibition of Src tyrosine kinase activity abrogated induction of gene expression. Furthermore, Src activity was necessary to maintain mRNA levels of FHOD1 itself, and as such, this finding represents the first description of mechanisms involved in the regulation of formin gene expression in mammals. In summary, we have identified Src as a key regulator of FHOD1 biology.
Insights
The study reveals that Src kinase is crucial for regulating formin homology domain containing protein 1 (FHOD1) functions. Src controls FHOD1
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- The formin FHOD1 protein impacts cell migration, cytoskeleton organization, and gene expression.
- Understanding FHOD1 regulation is key to deciphering its cellular roles.
Purpose of the Study:
- To investigate the regulatory role of Src in FHOD1-mediated cellular processes.
- To elucidate the mechanisms by which Src influences FHOD1 activity and expression.
Main Methods:
- Investigated FHOD1 localization in cells lacking Src.
- Analyzed stress fiber formation with truncated FHOD1 variants.
- Assessed gene expression from specific promoters.
- Examined the effect of Src inhibition on FHOD1-induced gene expression and FHOD1 mRNA levels.
Main Results:
- Src absence prevented FHOD1 localization to lamellipodia but did not affect stress fiber formation by truncated FHOD1.
- Src tyrosine kinase activity was essential for FHOD1-induced gene expression from SRE and skeletal actin promoters.
- Src activity maintained FHOD1 mRNA levels, indicating a regulatory feedback loop.
Conclusions:
- Src is identified as a critical regulator of FHOD1 biology.
- This study provides the first insights into the regulation of mammalian formin gene expression.
- Src influences FHOD1 localization, gene expression induction, and its own mRNA levels.
Related Concept Videos
Generation of Straight or Branched Actin Filaments
Arp2/3 Complex
Arp2/3 complex is a seven-subunit complex consisting of two proteins similar to actin- Arp2 and Arp3, and five other subunits that help keep Arp2 and Arp3 inactive. When required, the complex is...
Mechanism of Filopodia Formation
Their main function is to guide migrating cells during normal tissue morphogenesis or cancer metastasis by recognizing and making initial contacts with the extracellular matrix. However, they can also act as stationary cell anchors or help to establish communication...
Actin Filament Depolymerization
In F-actin, the ADF/cofilin proteins...
Pinching-off of Coated Vesicles
Restarting Stalled Replication Forks
Mechanism of Lamellipodia Formation

