Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Podocyte foot processes are supported by the actin cytoskeleton which is precisely organized by Rho GTPases. Rac1 and Cdc42 are the best characterized Rho GTPases in podocytes, and play a crucial role in cell adhesion, motility, polarity and survival. We recently reported that focal adhesion protein GIT2 suppresses Rac1 activity, thereby protecting podocytes against injury. However, the other isoform in mammals, GIT1, has not been investigated in the kidney including podocytes.
Podocyte-specific Git1 knockout mice were generated using the CRISPR/Cas9 system. Subsequently, podocyte-specific Git1 knockout mice were crossed with previously established systemic Git2 knockout mice (Shimada N, Matsuda J, et al; J Am Soc Nephrol. 2025) to generate double knockout mice. Immortalized human podocytes with GIT1/GIT2 single knockdown or double knockdown were established using lentiviral shRNA. Cell motility was monitored by tracking assay. Focal adhesion dynamics were analyzed using time-lapse fluorescence microscopy in cells transfected with mRFP-paxillin. Intracellular Rho GTPase activity and spatiotemporal dynamics were assessed by pull-down and Förster resonance energy transfer (FRET) assay.
Git1 knockout mice showed no overt phenotype under basal conditions and only mildly aggravated foot process effacement after injury. However, double knockout mice exhibited severe foot process effacement, late-onset albuminuria, podocyte detachment, and focal segmental glomerulosclerosis in adulthood. In cultured podocytes, GIT1 was localized at focal adhesions, similarly to GIT2. GIT2 knockdown or GIT1/GIT2 double knockdown, but not GIT1 knockdown alone, led to increased cell motility and accelerated focal adhesion turnover. Notably, motility of double knockdown podocytes lacked directionality and was accompanied by a significant reduction of Cdc42 activity especially at the cell edge. Mechanistically, the loss of Cdc42 activity in double knockdown podocytes was linked to enhanced degradation of the Cdc42-activating protein ARHGEF7, which was rescued by knockdown of the E3 ubiquitin ligase CBL-b. Furthermore, in double knockdown podocytes, ARHGEF7 was not properly localized in focal adhesions, which was rescued by re-expressing either GIT1 or GIT2.
GIT1 and GIT2 cooperatively maintain the ARHGEF7-Cdc42 signaling axis, highlighting a previously unrecognized mechanism regulating Rho GTPase activity and cytoskeletal organization in podocytes.
