SLC38A10 Deficiency in Mice Affects Plasma Levels of Threonine and Histidine in Males but Not in Females: A Preliminary Characterization Study of SLC38A10-/- Mice

Genes (Basel). 2023 Mar 30;14(4):835. doi: 10.3390/genes14040835.

Abstract

Solute carriers belong to the biggest group of transporters in the human genome, but more knowledge is needed to fully understand their function and possible role as therapeutic targets. SLC38A10, a poorly characterized solute carrier, is preliminary characterized here. By using a knockout mouse model, we studied the biological effects of SLC38A10 deficiency in vivo. We performed a transcriptomic analysis of the whole brain and found seven differentially expressed genes in SLC38A10-deficient mice (Gm48159, Nr4a1, Tuba1c, Lrrc56, mt-Tp, Hbb-bt and Snord116/9). By measuring amino acids in plasma, we found lower levels of threonine and histidine in knockout males, whereas no amino acid levels were affected in females, suggesting that SLC38A10-/- might affect sexes differently. Using RT-qPCR, we investigated the effect of SLC38A10 deficiency on mRNA expression of other SLC38 members, Mtor and Rps6kb1 in the brain, liver, lung, muscle, and kidney, but no differences were found. Relative telomere length measurement was also taken, as a marker for cellular age, but no differences were found between the genotypes. We conclude that SLC38A10 might be important for keeping amino acid homeostasis in plasma, at least in males, but no major effects were seen on transcriptomic expression or telomere length in the whole brain.

Keywords: SNAT10; amino acid homeostasis; gene expression analysis; knockout; solute carrier.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acids / metabolism
  • Animals
  • Female
  • Histidine* / genetics
  • Histidine* / metabolism
  • Humans
  • Liver / metabolism
  • Male
  • Membrane Transport Proteins / metabolism
  • Mice
  • Threonine* / metabolism

Substances

  • Histidine
  • Threonine
  • Amino Acids
  • Membrane Transport Proteins

Grants and funding

This study was supported by The Novo Nordisk Foundation, Swedish Research Council (DNR 2016/01972), Åhlens foundation, Gunvor and Josef Anérs foundation, Engkvist Foundation, The Swedish Brain Foundation and Magnus Bergvall Foundation.