bims-mitran 2026-04-19 papers

Issue of 2026–04–19
two papers selected by
Andreas Kohler, Umeå University

Mol Cell. 2026 Apr 16. pii: S1097-2765(26)00193-0. [Epub ahead of print]86(8): 1511-1528.e12

Mitochondrial translation elongation controls OXPHOS biogenesis by coordinating synthesis and folding of mitochondrially encoded proteins.

Lvxin Xie, Shuchao Ren, Li Zhang, Ziqing Wang, Tong Wu, Qing Dai, Shikun Xiang, Zhihua Qian, Yufan Xian, Shutong Xu, Xiao-Lin Chen, Chuan He, Yi Liu, Zhipeng Zhou.

Mitochondria generate ATP through oxidative phosphorylation (OXPHOS), with core structural subunits encoded by mitochondrial DNA (mtDNA) and translated by mitochondrial ribosomes. However, how mitochondrial translation elongation influences OXPHOS biogenesis remains unclear. Here, we show that in Neurospora crassa, the mitochondrial ribosomal RNA (rRNA) methyltransferase 1 (MRM1) promotes OXPHOS biogenesis by repressing translation elongation independently of its catalytic activity. The N-terminal intrinsically disordered region (IDR) of MRM1 binds simultaneously to mitochondrial ribosomes and mRNAs. Disrupting either interaction accelerates elongation and enhances synthesis of mtDNA-encoded OXPHOS subunits but impairs their co-translational folding and membrane insertion. Pharmacological slowing of mitochondrial translation partially alleviates these defects. The MRM1 IDR is conserved in Ascomycete fungi and is essential for plant infection by Magnaporthe oryzae. Together, our findings identify translation elongation control as a mechanism coordinating mitochondrial protein synthesis and folding during OXPHOS biogenesis and MRM1 as a potential target for broad-spectrum antifungal strategies.

Keywords: Magnaporthe oryzae; Neurospora crassa; mitochondrial rRNA methyltransferase; mitochondrial translation; oxidative phosphorylation; protein folding; translation elongation

DOI: https://doi.org/10.1016/j.molcel.2026.03.017

Autophagy. 2026 Apr 16. 1-3

A tRNA epitranscriptomic checkpoint coordinates sperm mitochondrial load with embryonic allophagic clearance.

Zhenhuan Luo, Qin-Li Wan, Dan Wu, Chenyang He, Tristan Argeo Rodriguez, Qinghua Zhou, Hao Wang.

The strict maternal inheritance of mitochondrial DNA is enforced by the efficient elimination of paternal mitochondria, yet the role of epigenetic regulation in this process remains unclear. In our recent study, we identify the demethylase ALKB‑1 as an essential factor for paternal mitochondrial elimination (PME) in Caenorhabditis elegans (C. elegans), functioning through tRNA m1A demethylation. ALKB‑1 deficiency leads to tRNA hypermethylation, which disrupts mitochondrial proteostasis and increases ROS production, thereby activating SKN‑1-ATFS‑1 stress signaling. This cascade compromises mitochondrial reduction during spermatogenesis, resulting in an increased burden of paternal mitochondria transmitted to the embryo. Concurrently, ALKB‑1 is required in the embryo to sustain autophagic clearance, evidenced by impaired autophagic flux and delayed PME upon maternal loss. Thus, delayed clearance stems dually from an excessive mitochondrial load in sperm and a compromised autophagic degradation capacity in the embryo. Our work establishes ALKB‑1‑dependent tRNA demethylation as a dual‑germline epitranscriptomic checkpoint that ensures intergenerational mitochondrial quality control.

Keywords: Allophagy; Caenorhabditis elegans; demethylase ALKB‑1; paternal mitochondrial elimination; tRNA m1A

DOI: https://doi.org/10.1080/15548627.2026.2659294