Abstract
<h3>Abstract</h3> Dyslexia is a common neurodevelopmental disorder with a strong genetic component. Independent genetic association studies have implicated the <i>KIAA0319</i> gene in dyslexia, however its function is still unknown. We developed a cellular knockout model for KIAA0319 in RPE1 cells via CRISPR-Cas9n to investigate its role in processes suggested but not confirmed in previous studies, including cilia formation and cell migration. We found that KIAA0319 knockout increased cilia length and accelerated cell migration. Using Elastic Resonator Interference Stress Microscopy (ERISM), we detected an increase in cellular force for the knockout cells that was restored by a rescue experiment. Combining ERISM and immunostaining showed that KIAA0319 depletion reduced the number of podosomes formed by the cells. Our results suggest an involvement of KIAA0319 in mechanosensing and force regulation and shows for the first time that podosomes exert highly dynamic, piconewton vertical forces in epithelial cells.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
