Discussion
The ribosome serves not only as a fundamental apparatus for protein synthesis but also plays a regulatory role in the process. One crucial component of the small ribosomal subunit, eS10, encoded by the RPS10 gene, has been implicated in mitochondrial function. Kwasniak-Owczarek et al. demonstrated through ribo-seq and RNA-seq analyses that defects in mitochondrial ribosomal protein S10, induced by RNAi, have profound effects on mitochondrial function in Arabidopsis. This study highlighted a marked down-regulation of mitochondrial oxidative phosphorylation and reduced translation efficiency of proteins associated with respiration upon RPS10 deficiency. Moreover, the study revealed that defects in mitochondrial ribosomal protein S10 also affect the translation of mitochondrial transcripts.
In this project, we aimed to get the altered mitochondrial gene expression profile observed in the aforementioned study. Through differential expression analysis using the edgeR package, we identified several differentially expressed genes (DEGs) in Arabidopsis, notably MATR, RPL16, RPS4, RPS12, TATC, and RPL5, most of which are related to ribosomes. The volcano plot representation illustrated the significant changes in gene expression levels caused by RPS10 gene knockdown.
GO enrichment analysis of the DEGs shed light on the biological effects of RPS10 silencing. The results revealed alterations in genes involved in proton-transporting ATP synthase complex, mitochondrial membrane, ribosome, proton transmembrane transport, oxidative phosphorylation, and oxidoreduction-driven active transmembrane transporter activity. This suggests a broad impact of RPS10 dysregulation on mitochondrial function and energy metabolism.
Furthermore, by matching the DEGs in Arabidopsis to their human orthologs, we conducted a functional enrichment analysis on the human homologs. The analysis indicated enrichment in mitochondrial protein-containing complex, mitochondrial inner membrane, ribosomal subunit, ribosome, ribose phosphate biosynthetic process, proton motive force-driven mitochondrial ATP synthesis, aerobic respiration, and oxidative phosphorylation. These findings suggest conservation of function across species and imply potential relevance to human mitochondrial biology and associated diseases.
Additionally, KEGG pathway analysis on the human orthologs identified several signaling pathways affected by aberrant RPS10 expression, including oxidative phosphorylation, diabetic cardiomyopathy, chemical carcinogenesis-reactive oxygen species, thermogenesis, ribosome, and neurodegenerative diseases such as Parkinson's, Alzheimer's, and Huntington's diseases. These results provide insights into the potential mechanisms underlying RPS10-mediated regulation and its implications for human health.
 Conclusion
In this study, we have investigated the regulatory role of mitochondrial ribosomal protein S10 (RPS10) in Arabidopsis and its potential implications for human mitochondrial function and health. Through differential expression analysis and functional enrichment studies, we have demonstrated that RPS10 deficiency leads to significant alterations in mitochondrial gene expression profiles, particularly affecting genes involved in oxidative phosphorylation, ribosome function, and proton transport. These findings underscore the critical role of RPS10 in maintaining mitochondrial function and energy metabolism.
Furthermore, our identification of human orthologs of differentially expressed genes in Arabidopsis suggests a conservation of function across species. Functional enrichment analysis of these human homologs reveals their involvement in key biological processes and pathways related to mitochondrial function, energy production, and disease pathways. This implies that insights gained from studying RPS10 in Arabidopsis may have relevance to human mitochondrial biology and could offer new avenues for understanding and potentially treating mitochondrial disorders.
Overall, our study provides valuable insights into the molecular mechanisms underlying RPS10-mediated regulation of mitochondrial function. By elucidating the impact of RPS10 dysregulation on gene expression profiles and signaling pathways, we contribute to a deeper understanding of mitochondrial dysfunction and its implications for human health. These findings lay the groundwork for future research aimed at further dissecting the role of RPS10 in mitochondrial biology and exploring its potential as a therapeutic target for mitochondrial diseases.