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Lowering dietary BCAA reduces fibrosis, enhances mitochondrial respiration, and curbs cardiac hypertrophy, via regulating histone H3K23-propionylation

ABSTRACT: Lowering dietary BCAA reduces fibrosis, enhances mitochondrial respiration, and curbs cardiac hypertrophy, via regulating histone H3K23-propionylation

PROVIDER: PRJNA953006 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23848232.fastq.gz	Fastqsanger.gz
	SRR23848233.fastq.gz	Fastqsanger.gz
	SRR23848234.fastq.gz	Fastqsanger.gz
	SRR23848235.fastq.gz	Fastqsanger.gz
	SRR23848236.fastq.gz	Fastqsanger.gz

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Project description:Identifying branched-chain amino acid (BCAA) oxidation enzymes in the nucleus led us to predict that they are a source of propionyl-CoA that could be utilized for histone propionylation and, thereby, regulate gene expression. To investigate this and its effect on the development of cardiac hypertrophy and failure, we applied pressure overload on the heart in mice maintained on a diet with standard levels of BCAA (BCAA-control) versus a BCAA-free diet. The former was associated with an increase in H3K23-propionyl (H3K23Pr) at the promoters of upregulated genes [e.g., cell signaling and extracellular matrix (ECM) genes] and a decrease at the promoters of downregulated genes [e.g., electron transfer complex (ETC I-V) and metabolic genes]. Intriguingly, the BCAA-free diet diminished the increase in promoter-H3K23Pr and significantly reduced ECM gene expression and collagen deposition. Conversely, the BCAA-free diet abolished the downregulation of ETC I-V subunits, enhanced mitochondrial respiration, and curbed cardiac hypertrophy. Thus, lowering the intake of BCAA reduces histone propionylation, which moderates the effects of stress on the heart.

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Project description:We used RNA-Seq to ask whether the transcripts for the proposed BCKDH subunits are upregulated in wild-type plants subjected to prolonged darkness. These experiments were performed using rosette leaves from 5-week-old, short-day-grown (8h light/16h dark) Col-0 wild-type plants moved to constant darkness for 6h, 24h, 48h and 72h, and grown in short day for 72h as control. The transcripts of eight BCAA catabolism genes were increased nine- to 400-fold within the first 6h of prolonged darkness, and remained high until the last time point. These results are consistent with the hypothesis that BCAA catabolic enzymes - including BCKDH subunits E1A1, E1B1, E1B2 and E2 - have one or more physiological roles in the dark. Rosette leaf mRNA profiles of 5-week old Col wild type (WT, CS60000) and BCAA catabolic mutants ivd1-2 and hml1-2 were generated byRNA sequencing, in duplicate, using Illumina HiSeq2500.

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