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Mitochondrial precursors are partially unfolded or loosely folded polypeptide chains. Newly synthesized precursors are inhibited from spontaneously folding into their native conformation by the cytosolic chaperones, heat shock proteins 70 (Hsp70), and mitochondrial import stimulation factors (MSFs). Precursors bound to MSFs are guided to the TOM70-TOM37 receptors, while precursors bound to Hsp70  chaperones are targetted to TOM20-TOM22 receptor complexes.
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Cardiac mitochondrial function depends on BUD23 mediated ribosome programming.

Matthew Baxter1,2,3, Maria Voronkov1,2,3, Toryn Poolman1,2,3

  • 1Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, United Kingdom.

Elife
|January 16, 2020
PubMed
Summary
This summary is machine-generated.

The study reveals BUD23 is crucial for ribosome generation, impacting mitochondrial protein translation. Its absence causes severe heart dysfunction and developmental issues in mice.

Keywords:
cardiaccell biologyhumanmitochondriamouseprotein translationribosome

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cardiovascular Science

Background:

  • Mitochondrial function is vital for high-energy tissues like the heart.
  • Mitochondrial dysfunction is linked to cardiovascular diseases.
  • Mitochondrial protein expression requires tight regulation.

Purpose of the Study:

  • To identify novel mechanisms regulating mitochondrial content and function.
  • To investigate the role of BUD23 in ribosome generation and mitochondrial gene expression.
  • To determine the impact of BUD23 on cardiac function and development.

Main Methods:

  • Investigated BUD23's role in ribosome maturation and mitochondrial transcript translation in human A549 cells.
  • Deleted BUD23 in murine cardiomyocytes to assess effects on mitochondrial content and function.
  • Analyzed BUD23's interaction with 5'UTRs of varying GC content.

Main Results:

  • BUD23 is essential for ribosome maturation and normal 18S/28S stoichiometry.
  • BUD23 deletion in cardiomyocytes reduced mitochondrial content and function, causing cardiomyopathy and death.
  • BUD23 selectively promotes ribosomal interaction with low GC-content 5'UTRs, enhancing translation of specific mRNAs.

Conclusions:

  • BUD23 plays a critical role in bioenergetics gene expression by facilitating translation of mRNAs with low 5'UTR GC content.
  • BUD23 is essential for mouse development and postnatal cardiac function.
  • BUD23-dependent ribosome generation is a novel mechanism regulating mitochondrial content and function.