Document Type

Article

Publication Date

6-1-2024

Keywords

JMG, SS1, Animals, Mice, Actins, Autophagy, Mice, Knockout, Humans, Autophagosomes, Kidney, Male, Kidney Tubules, Proximal, Actin Cytoskeleton, Actin-Related Protein 2-3 Complex, Membrane Proteins, Microtubule-Associated Proteins, Polymerization, Fibroblasts

JAX Source

Mol Biol Cell. 2024;35(6):ar80.

ISSN

1939-4586

PMID

38598293

DOI

https://doi.org/10.1091/mbc.E24-01-0025

Grant

R.K. was sup- ported by National Institutes of Health grants ES29916, AG038070, DK131019, and DK131061, and the Alport Syndrome Foundation

Abstract

The actin cytoskeleton is essential for many functions of eukaryotic cells, but the factors that nucleate actin assembly are not well understood at the organismal level or in the context of disease. To explore the function of the actin nucleation factor WHAMM in mice, we examined how Whamm inactivation impacts kidney physiology and cellular proteostasis. We show that male WHAMM knockout mice excrete elevated levels of albumin, glucose, phosphate, and amino acids, and display structural abnormalities of the kidney proximal tu- bule, suggesting that WHAMM activity is important for nutrient reabsorption. In kidney tis- sue, the loss of WHAMM results in the accumulation of the lipidated autophagosomal mem- brane protein LC3, indicating an alteration in autophagy. In mouse fibroblasts and human proximal tubule cells, WHAMM and its binding partner the Arp2/3 complex control autopha- gic membrane closure and cargo receptor recruitment. These results reveal a role for WHAMM-mediated actin assembly in maintaining kidney function and promoting proper au- tophagosome membrane remodeling.

Creative Commons License

Creative Commons Attribution 4.0 International License
This work is licensed under a Creative Commons Attribution 4.0 International License.

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