Background:The regulation of multi-functional DYNLL1 is poorly understood. Results: ASCIZ activates Dynll1 gene expression and is inhibited by DYNLL1 binding to its transcription activation domain. Conclusion: ASCIZ plays a key role in the auto-regulation of DYNLL1 levels. Significance: This is the first case where a gene product directly inhibits its main transcriptional activator while bound at its own promoter.

B cell development requires the Zinc-finger protein and ATM substrate ASCIZ to signal through DYNLL1 and Bim.