DPYSL2, also known as CRMP2, encodes a microtubule-stabilizing protein of great significance in neurogenesis. It is associated with multiple pathways such as mTOR signaling, cytoskeletal dynamics, immune function, calcium signaling, and cholesterol biosynthesis [1,3,5]. This gene is linked to numerous psychiatric and neurodegenerative disorders, including schizophrenia, bipolar disorder, and Alzheimer's disease, highlighting its overall biological importance [1]. Genetic models, like knockout models, have been crucial in understanding its functions.

In human iPSC-derived glutamatergic neurons, knockout of DPYSL2-B (an isoform of DPYSL2) led to a reduction in dendrite length and disruptions in pathways relevant to psychiatric diseases, confirming its role in mTOR signaling and neurodevelopmental disorders [1]. In zebrafish, dpysl2 knockout caused abnormal migration of facial branchiomotor neurons during early development [4]. In breast cancer cells, DPYSL2 knockout profoundly inhibited cell migration, invasion, stemness features, tumor growth rate, and metastasis [2].

In conclusion, DPYSL2 is essential for neurogenesis, neuronal migration, and has an impact on cancer cell behavior. Gene knockout models, especially in neurons and zebrafish, have been instrumental in revealing its role in neurodevelopmental disorders and cancer-related processes, providing valuable insights into the underlying molecular mechanisms of these diseases.