Myo1c-KO Mouse

Myo1c, also known as myosin1c, is an unconventional myosin motor protein. It is involved in various cellular processes such as cytoskeleton remodeling, intracellular transport, and vesicle tethering, which are crucial for normal cell function and tissue homeostasis. It is associated with pathways like TGF-β signaling, and its functions impact diverse biological processes in multiple tissues [1,2]. Genetic models, including gene knockout models, have been instrumental in understanding Myo1c's functions.

In podocyte-specific Myo1c knockout mice, resistance to fibrotic injury induced by Adriamycin or nephrotoxic serum was observed, suggesting Myo1c's role in TGF-β-signaling-mediated podocyte disease pathogenesis [2]. Systemic loss of Myo1c in mice led to rhodopsin mislocalization and impaired visual function [3]. In zebrafish, Myo1c knockdown caused abnormal podocyte morphology, absence of the slit diaphragm, and altered glomerular filter permeability, indicating its necessity for podocyte morphogenesis [4].

In conclusion, Myo1c is essential for multiple biological functions, including maintaining normal podocyte function, visual function, and glomerular development. Gene knockout models in mice and zebrafish have been pivotal in revealing its role in fibrotic diseases, visual impairment, and podocyte-related pathologies, providing insights into potential therapeutic targets for these conditions.

References:

1. Liu, Di, Li, Ruiru, Xu, Siqi, Xiao, Youjun, Xu, Hanshi. 2022. SMOC2 promotes aggressive behavior of fibroblast-like synoviocytes in rheumatoid arthritis through transcriptional and post-transcriptional regulating MYO1C. In Cell death & disease, 13, 1035. doi:10.1038/s41419-022-05479-0. https://pubmed.ncbi.nlm.nih.gov/36513634/

2. Arif, Ehtesham, Solanki, Ashish K, Srivastava, Pankaj, Kwon, Sang-Ho, Nihalani, Deepak. 2019. The motor protein Myo1c regulates transforming growth factor-β-signaling and fibrosis in podocytes. In Kidney international, 96, 139-158. doi:10.1016/j.kint.2019.02.014. https://pubmed.ncbi.nlm.nih.gov/31097328/

3. Solanki, Ashish K, Biswal, Manas R, Walterhouse, Stephen, Nihalani, Deepak, Lobo, Glenn Prazere. 2021. Loss of Motor Protein MYO1C Causes Rhodopsin Mislocalization and Results in Impaired Visual Function. In Cells, 10, . doi:10.3390/cells10061322. https://pubmed.ncbi.nlm.nih.gov/34073294/

4. Arif, Ehtesham, Kumari, Babita, Wagner, Mark C, Holzman, Lawrence B, Nihalani, Deepak. 2013. Myo1c is an unconventional myosin required for zebrafish glomerular development. In Kidney international, 84, 1154-65. doi:10.1038/ki.2013.201. https://pubmed.ncbi.nlm.nih.gov/23715127/