bims-micpro 2021-08-01 papers

Interdiscip Sci. 2021 Jul 25.

LncRNA-Encoded Short Peptides Identification Using Feature Subset Recombination and Ensemble Learning.

Long non-coding RNA (lncRNA), which is a type of non-coding RNA, was reported to contain short open reading frames (sORFs). SORFs-encoded short peptides (SEPs) have been demonstrated to play a crucial role in regulating the biological processes such as growth, development, and resistance response. The identification of SEPs is vital to further understanding their function. However, there is still a lack of methods for identifying SEPs effectively and rapidly. In this study, a novel method for lncRNA-encoded short peptides identification based on feature subset recombination and ensemble learning, lncPepid, is developed. lncPepid transforms the data of Zea mays and Arabidopsis thaliana into hybrid features from two aspects including sequence composition and physicochemical properties separately. It optimizes hybrid features by proposing a novel weighted iteration-based feature selection method to recombine a stable subset that characterizes SEPs effectively. Different classification models with different optimized features are constructed and tested separately. The outputs of the optimal models are integrated for ensemble classification to improve efficiency. Experimental results manifest that the geometric mean of sensitivity and specificity of lncPepid is about 70% on the identification of functional SEPs derived from multiple species. It is an effective and rapid method for the identification of lncRNA-encoded short peptides. This study can be extended to the research on SEPs from other species and have crucial implications for further findings and studies of functional genomics.

Keywords: Ensemble learning; Feature subset recombination; Long non-coding RNA; Short open reading frames; Short peptides

DOI: https://doi.org/10.1007/s12539-021-00464-1

J Bacteriol. 2021 Jul 26. JB0034121

Small Proteins; Big Questions.

Todd Gray, Gisela Storz, Kai Papenfort.

In recent years there has been increased appreciation that a whole category of proteins-small proteins of around 50 amino acids or fewer in length-have been missed by annotation as well as by genetic and biochemical assays. With the increased recognition that small proteins are stable within cells and have regulatory functions, there has been intensified study of these proteins. As a result, important questions about small proteins in bacteria and archaea are coming to the fore. Here, we give an overview of these questions, the initial answers, and the approaches needed to address the questions more fully. More detailed discussions of how small proteins can be identified by ribosome profiling and mass spectrometry approaches are provided by two accompanying reviews. We are excited by the prospects of new insights and possibly therapeutic approaches coming from this emerging field.

DOI: https://doi.org/10.1128/JB.00341-21

Cell Rep. 2021 Jul 27. pii: S2211-1247(21)00864-0. [Epub ahead of print]36(4): 109447

Mitochondrial-encoded MOTS-c prevents pancreatic islet destruction in autoimmune diabetes.

Byung Soo Kong, Se Hee Min, Changhan Lee, Young Min Cho.

Mitochondria are principal metabolic organelles that are increasingly unveiled as immune regulators. However, it is currently not known whether mitochondrial-encoded peptides modulate T cells to induce changes in phenotype and function. In this study, we found that MOTS-c (mitochondrial open reading frame of the 12S rRNA type-c) prevented autoimmune β cell destruction by targeting T cells in non-obese diabetic (NOD) mice. MOTS-c ameliorated the development of hyperglycemia and reduced islet-infiltrating immune cells. Furthermore, adoptive transfer of T cells from MOTS-c-treated NOD mice significantly decreased the incidence of diabetes in NOD-severe combined immunodeficiency (SCID) mice. Metabolic and genomic analyses revealed that MOTS-c modulated T cell phenotype and function by regulating T cell receptor (TCR)/mTOR complex 1 (mTORC1) signaling. Type 1 diabetes (T1D) patients had a lower serum MOTS-c level than did healthy controls. Furthermore, MOTS-c reduced T cell activation by alleviating T cells from the glycolytic stress in T1D patients, suggesting therapeutic potential. Our findings indicate that MOTS-c regulates the T cell phenotype and suppresses autoimmune diabetes.

Keywords: CD4(+) T cell; Foxp3; IFNγ; MOTS-c; T cell activation; T cell differentiation; T(reg); mTORC1; mitochondria; type 1 diabetes

DOI: https://doi.org/10.1016/j.celrep.2021.109447