Dynlrb1, also known as Dynein Light Chain Roadblock-Type 1, is an essential subunit of the dynein complex. It plays a crucial role in dynein-mediated transport, which is vital for the survival and function of highly polarized cells like neurons. Dynlrb1 is involved in multiple signaling pathways, such as the β-catenin subcellular localization pathway, and is associated with the axonal transport of lysosomes and retrograde signaling endosomes [1].

Homozygous Dynlrb1 null mice are not viable and die during early embryonic development [1]. Heterozygous or adult knockdown animals display reduced neuronal growth, and selective depletion of Dynlrb1 in proprioceptive neurons compromises their survival [1]. Conditional depletion of Dynlrb1 in sensory neurons causes deficits in several signaling pathways and severe impairment in axonal transport [1]. In addition, in male meiosis, the ubiquitously expressed Dynlrb1 maintains spindle bipolarity by targeting NuMA and suppressing centriole overduplication, while a related protein Dynlrb2 has a similar role specifically in male meiotic spindle formation [2].

In conclusion, Dynlrb1 is essential for general dynein-mediated transport and neuronal survival. Studies using Dynlrb1 knockout mouse models have revealed its critical role in early embryonic development and neuronal functions. Given dynein's key functions in neuronal physiology, Dynlrb1 could potentially play a prominent role in the etiology of human neurodegenerative diseases [1].