Mice overexpression of <i>human augmenter of liver regeneration</i> (hALR) in male germ cells shows abnormal spermatogenesis and reduced fertility

Mettl3-/Mettl14-mediated mRNA N6-methyladenosine modulates murine spermatogenesis

“…Interestingly, in mutant spermatocytes, genes with TE up-regulated include many factors for DNA replication and repair, which are required for early stage of spermatocytes but unnecessary for pachytenes (Supplementary information, Table S7), suggesting that m 6 A may repress translation of overexpressed transcripts to prevent protein overproduction. Accordingly, in male germ cells, overexpression of Gfer, one of the genes with TE up-regulated, has been reported to cause male infertility [55]. Taken together, these results support the idea that m 6 A modification could serve as a mark to promote translation for producing proteins essential for spermiogenesis, and inhibit translation for preventing deleterious consequences of overproducing proteins during late spermatogenesis.…”

Augmenter of liver regeneration: A fundamental life protein

“…(44) This essay has touched upon the myriad roles of ALR in selected basic life processes. Additional roles in spermatogenesis, where it is expressed at highest levels, (45) or in the CNS, in which it has been mapped to all parts of the brain (46) but remains unstudied, represent further areas of investigation. New tools such as a specific ALR inhibitor (31) may lead to more focused studies in the near future.…”

Recombinant human augmenter of liver regeneration protects hepatocyte mitochondrial DNA in rats with obstructive jaundice

“…Indeed, ALR may act through other mechanisms, and further studies are needed. For example, it is known that ALR can be used to protect against oxidative damage caused by ROS [16,47], and that ROS is a major cause of mtDNA damage [48]. Our future studies will aim toward discriminating this indicator and/or cause duality.…”