MAP1S, also known as microtubule-associated protein 1 small form (originally named C19ORF5), is a significant protein. It serves as linkers connecting mitochondria with microtubules for trafficking and bridges the autophagy machinery with microtubules and mitochondria, influencing autophagosomal biogenesis and degradation. MAP1S is involved in pathways like cell division, autophagy, phagocytosis, and Toll-like receptor (TLR) signaling, which are crucial for normal cellular function and immune defense [1,2,3]. Genetic models, such as gene knockout mouse models, can be valuable for studying its functions.

In KO mouse models, MAP1S deficiency leads to various issues. For example, in mice with MAP1S deleted, there is an impairment of autophagy clearance of fibronectin in renal cells, leading to an accumulation of fibrosis-related proteins and the development of renal fibrosis in aged mice [4]. In another case, defects in MAP1S-mediated autophagy in mice trigger oxidative stress, sinusoidal dilation, and lifespan reduction, especially when fibronectin is overexpressed [5].

In conclusion, MAP1S plays essential roles in maintaining microtubule stability during cell division, regulating autophagy, phagocytosis, and TLR signaling. Studies using KO mouse models have revealed its significance in diseases like renal fibrosis and in maintaining normal physiological states such as lifespan. These insights into MAP1S functions contribute to a better understanding of related biological processes and disease mechanisms, potentially guiding future research for therapeutic interventions.