Background: The SWI/SNF complex is a central ATPase dependent chromatin remodeling complex that is conserved from yeast to humans.The genes encoding the core homologues of the yeast SWI/SNF complex in Drosophila include the Bap complex brahma (brm), moira (mor) and osa.In a RNAi screen for genes that affect heart function in Drosophila mor and osa were identified.However, how chromatin remodeling affects cardiac function in adult Drosophila remains unknown.Results: In flies with heart-specific knockdown (KD) of brm,mor or osa, we have observed a decreased heart rate (prolonged Systolic and Diastolic Interval, SI, DI), increased Arrhythmia Index (AI) and compromised contractility (decreased Fractional Shortening, FS).Immuno-staining has also shown disorganized myofibrils and even some gaps in posterior heart chambers consistent with the observed decrease in contractility.Intriguingly, cardiac-specific knockdown (KD) of brm, mor and osa produce similar phenotypes that are not further aggravated in with double KD, suggesting that each single KD strongly disrupts the entire BAP complex.These phenotypes tend to be further aggravated with age, suggesting that Bap complexdependent chromatin remodeling is required to prevent pre-mature cardiac senescence.To identify downstream effectors of the Bap complex in regulating heart function, we performed microarray analysis of brm, mor and osa KD hearts.We find that numerous proteasome complex components were highly enriched among the downregulated genes in one or more Bap complex KD hearts, including the proteasome regulatory components Rpn11and Rpn2.Significantly, overexpression of Rpn11 partially rescues cardiac dysfunction of Bap complex KD hearts,and cardiac KD of Rpn1 1 mimics the phenotype of Bap complex KD, suggesting that Rpn11 may be a downstream effector of the Bap complex.Interestingly, overexpression of Rpn11 in wildtype hearts ameliorates the decline in heart function with age, eg.by reducing AI in old flies, which implicates proteasomal-mediated proteostasis and possibly chromatin remodeling in cardiac senescence.Conclusion: Our study suggests that the Bap complex components and transcriptional regulation of downstream proteasome components are required for maintaining normal heart function, and that Rpn11 is likely a critical link between chromatin remodeling and proteostasis to regulate heart function and prevent premature cardiac senescence.