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Parkin-mediated mitophagy evokes perinatal cardiac mitochondria maturation

ABSTRACT: Exclusion of Parkin from mitochondria of perinatal cardiomyocytes interrupts structural and molecular transformations essential to normal perinatal-adult mitochondrial replacement. mRNA-sequencing from cardiac total RNA was performed at P1, P21 and 5-week stages of nontransgenic (ntg) and human-Mfn2-overexpressing (Mfn2wt) hearts, and also of tet-off control (tetoff) and human-Mfn2 T111A/S442A-overexpressing (Mfn2AA) hearts. Libraries from all P1 samples were prepared and analyzed together, and similarly all P21 libraries, and all 5-week libraries together. To facilitate comparison across time points by accounting for batch effect, new libraries were prepared starting from total RNA from selected P21 ntg and 5-week ntg hearts subjected to prior analysis, during the same batch preparation as all P1 samples, and analyzed together. Correction for differences observed between libraries prepared from the same total RNA, but at different times, allows comparison across timepoints.

ORGANISM(S): Mus musculus

SUBMITTER: Scot Matkovich 

PROVIDER: E-GEOD-68921 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Parkin-mediated mitophagy directs perinatal cardiac metabolic maturation in mice.

Gong Guohua G   Song Moshi M   Csordas Gyorgy G   Kelly Daniel P DP   Matkovich Scot J SJ   Dorn Gerald W GW  

Science (New York, N.Y.) 20151203 6265

In developing hearts, changes in the cardiac metabolic milieu during the perinatal period redirect mitochondrial substrate preference from carbohydrates to fatty acids. Mechanisms responsible for this mitochondrial plasticity are unknown. Here, we found that PINK1-Mfn2-Parkin-mediated mitophagy directs this metabolic transformation in mouse hearts. A mitofusin (Mfn) 2 mutant lacking PINK1 phosphorylation sites necessary for Parkin binding (Mfn2 AA) inhibited mitochondrial Parkin translocation, s  ...[more]

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