NUDC, also known as nuclear distribution protein C, is a mitotic protein involved in nuclear migration and cytokinesis across species. Considered a cytoplasmic dynein cofactor, it associates with the dynein motor complex. It's also expressed in postmitotic vertebrate rod photoreceptors. Its role in maintaining cell division and potentially in related cellular pathways is of biological importance, and genetic models like knockout mice are valuable for studying its functions [1,2,3,4,5].

In conditional NUDC knockout mouse rods (rNudC -/-), loss of NUDC led to complete photoreceptor cell death at six weeks of age. By three weeks, rNudC -/- function was diminished, with mislocalization of rhodopsin and mitochondria, reduced outer segment proteins, and ultrastructural defects, consistent with dynein inhibition. NUDC may interact with the actin modulator cofilin 1 (CFL1), as loss of NUDC increased phosphorylated CFL1 levels, preventing actin depolymerization. Also, NUDC absence induced an inflammatory response in Müller glia and microglia across the neural retina by three weeks [1,2].

In conclusion, NUDC is crucial for actin cytoskeletal maintenance and dynein-mediated protein trafficking in postmitotic rod photoreceptors. The rNudC -/- mouse model has revealed its significance in preventing photoreceptor cell death and maintaining normal function, providing insights into potential mechanisms underlying retinal degeneration-related diseases [1,2].