The non-catalytic function of BRM negatively impacts CLK binding to the <i>per</i> promoter.

<p>ChIP assays detecting CLK binding at the <i>(A-B) per</i> CRS and <i>(C-D) tim</i> E-box 1 in flies expressing (<i>A</i> and <i>C</i>) catalytically-inactive <i>brm</i>^<i>K804R</i> and (<i>B</i> and <i>D</i>) <i>brm</i> RNA<i>i</i> (v37720) in <i>tim</i>-expressing cells as compared to control <i>TUG(II)</i> and <i>TUG</i> flies. Corresponding ChIP assays detecting PER binding at the (<i>E-F</i>) <i>per</i> CRS and (<i>G-H</i>) <i>tim</i> E-box 1 in flies expressing (<i>E</i> and <i>G</i>) <i>brm</i>^<i>K804R</i> and (<i>F</i> and <i>H</i>) <i>brm</i> RNA<i>i</i> as compared to control <i>TUG(II)</i> and <i>TUG</i> flies. Results shown are from at least three biological ChIP replicates, with technical triplicates performed during qPCR for each biological replicate. Error bars = SEM of biological replicates. Asterisks denote significant difference between control and <i>brm</i> mutant at indicated time points (P < 0.05).