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Updated: Jan 31, 2026

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ALKB-1-dependent tRNA methylation is required for efficient paternal mitochondrial elimination.

Zhenhuan Luo1,2,3, Yimin Li4,5, Chenyang He2,3,5

  • 1Department of Cardiology, The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, China.

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|January 29, 2026
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The DNA/RNA demethylase ALKB-1 is crucial for removing paternal mitochondria during reproduction in C. elegans. Its absence disrupts mitochondrial quality control, impacting fertility and embryonic development.

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Area of Science:

  • Epigenetics and Developmental Biology
  • Mitochondrial Biology
  • Reproductive Science

Background:

  • Maternal inheritance of mitochondria relies on eliminating paternal mitochondria.
  • The role of epigenetic modifications in paternal mitochondrial elimination (PME) is not well understood.
  • Understanding PME is key to reproductive success and preventing mitochondrial diseases.

Purpose of the Study:

  • To investigate the role of epigenetic modifications in paternal mitochondrial elimination (PME).
  • To identify key factors regulating mitochondrial quality control during reproduction.
  • To elucidate the mechanisms underlying the inheritance of mitochondria.

Main Methods:

  • Utilized Caenorhabditis elegans (C. elegans) as a model organism.
  • Investigated the function of the DNA/RNA demethylase ALKB-1 in PME.
  • Analyzed the impact of ALKB-1 on tRNA m1A methylation, protein translation, mitochondrial proteostasis, and ROS levels.
  • Examined the activation of oxidative stress response (SKN-1/Nrf2) and mitochondrial unfolded protein response (UPRmt) pathways.

Main Results:

  • ALKB-1 is essential for efficient paternal mitochondrial elimination (PME).
  • ALKB-1 inactivation causes tRNA m1A hypermethylation, disrupting protein translation and mitochondrial proteostasis.
  • Impaired PME leads to increased ROS, activation of SKN-1/Nrf2 and UPRmt, and accumulation of mitochondria and mtDNA in sperm.
  • Defects in PME negatively affect male fertility and embryonic development.

Conclusions:

  • ALKB-1-mediated tRNA m1A epitranscriptomic modifications are critical for mitochondrial quality control and PME.
  • This epitranscriptomic stress checkpoint ensures proper mitochondrial inheritance during reproduction.
  • Dysregulation of ALKB-1 impacts male fertility and embryonic outcomes, highlighting its importance in reproductive health.