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Abstract
BMAL1 is SUMOylated on a conserved lysine residue (Lys259) in vivo, demonstrating a circadian pattern of modification.
- SUMOylation of BMAL1 correlates with its activation in the mouse liver.
- The process of SUMOylation is dependent on CLOCK, which partners with BMAL1.
- Ectopic expression of a SUMO-deficient BMAL1 suggests that SUMOylation is important for BMAL1's circadian expression.
- These findings indicate a new regulatory layer in the core mechanism of the circadian clock.
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