Normal mitochondrial function in Saccharomyces cerevisiae has become dependent on inefficient splicing.

Area of Science:

• Molecular Biology
• Genetics
• Cell Biology

Background:

• Self-splicing introns are mobile genetic elements found in prokaryotic and organellar genomes.
• Their presence in conserved genes suggests a complex evolutionary history.

Purpose of the Study:

• To investigate the impact of removing self-splicing introns from the Saccharomyces cerevisiae mitochondrial genome.
• To understand the role of these introns in host cell physiology and gene expression.

Main Methods:

• Generating a yeast strain lacking mitochondrial introns.
• Analyzing mitochondrial morphology, gene expression, and metabolic profiles.
• Overexpressing the splicing factor Mss116 to mimic intron deletion effects.

Main Results:

• Mitochondrial intron deletion induced a retrograde response, affecting morphology, gene expression, and metabolism.
• Growth and lifespan were negatively impacted in intron-deleted strains.
• Overexpression of Mss116 phenocopied intron deletion, leading to excess mature cob and cox1 mRNA.

Conclusions:

• Inefficient splicing due to self-splicing introns is integral to normal yeast mitochondrial gene expression.
• Subsequent intron loss is deleterious, suggesting an evolutionary 'lock-in' mechanism.
• Host genome adaptation to early intron invasion rendered later loss detrimental.