Fndc-1 contributes to paternal mitochondria elimination in C. elegans

Area of Science:

• Cell Biology
• Genetics
• Developmental Biology

Background:

• Paternal mitochondria are eliminated post-fertilization via selective autophagy, a process critical for preventing mitochondrial inheritance.
• The precise mechanisms ensuring the selective degradation of sperm-derived mitochondria remain incompletely understood.
• FUNDC1 (FUN14 domain containing 1) is a known mammalian mitophagy receptor involved in mitochondrial quality control under hypoxia.

Purpose of the Study:

• To investigate the role of the C. elegans ortholog FNDC-1 in paternal mitochondria elimination.
• To determine if FNDC-1 mediates the selective degradation of sperm mitochondria in nematodes.

Main Methods:

• Utilized CRISPR/Cas9 to generate fndc-1 loss-of-function mutants in C. elegans.
• Examined paternal mitochondrial DNA transmission in offspring from wild-type and fndc-1 mutant crosses.
• Assessed the degradation rates of paternal mitochondria and membranous organelles in fndc-1 mutants.

Main Results:

• FNDC-1 is highly expressed in C. elegans sperm but not oocytes.
• Loss of fndc-1 function in males results in detectable paternal mitochondrial DNA in larvae.
• fndc-1 mutation delays paternal mitochondria degradation but does not affect membranous organelles.

Conclusions:

• FNDC-1 is essential for the efficient elimination of paternal mitochondria in C. elegans.
• This study identifies a ubiquitin-independent mitophagy receptor involved in selective sperm mitochondria degradation.
• FNDC-1 plays a specific role in sperm mitochondria turnover, distinct from membranous organelle degradation.