bims-micpro Biomed News
on Discovery and characterization of microproteins
Issue of 2026–02–01
seven papers selected by
Thomas Farid Martínez, University of California, Irvine



  1. J Endocrinol Invest. 2026 Jan 27.
      Adipose tissue exhibits remarkable plasticity, defined as its capability of adapting to various environments and energy demands by undergoing shifts in phenotypic, metabolic characteristics, and structure. However, obesity often results in diminished adipose tissue plasticity. Long non-coding RNA (lncRNA) is a class of RNA defined as being more than 200 nucleotides long and lacking protein-coding capability. With advancements in ribosome profiling, mass spectrometry, and other research technologies, an increasing number of studies have confirmed that short open reading frames (less than 300 nucleotides) within lncRNAs have the capacity to encode functional micropeptides. In our study, we initially identified a biologically active micropeptide, lncRNA Esrp2-as-ORF1(LEAO), encoded by lncRNA Esrp2-as in mice. In diet-induced obesity (DIO)mice, this micropeptide demonstrates the ability to induce fat browning, enhance adipose tissue plasticity, and subsequently improve metabolic homeostasis. Additionally, we observed that the micropeptide LEAO exerts its effects on adipocytes by stimulating IL6 secretion in adipose tissue macrophages. In summary, LEAO may have therapeutic potential for obesity-related metabolic diseases.
    Keywords:  Adipose tissue; Esrp2-as; LncRNA; Micropeptide; Obesity
    DOI:  https://doi.org/10.1007/s40618-026-02813-7
  2. Cells. 2026 Jan 20. pii: 188. [Epub ahead of print]15(2):
      Cells are continuously exposed to physiological and environmental stressors that disrupt homeostasis, triggering adaptive mechanisms such as the integrated stress response (ISR). A central feature of ISR is the selective translation of activating transcription factor 4 (ATF4), which orchestrates gene programs essential for metabolic adaptation and survival. Stress-induced acute ATF4 expression occurs in diverse mammalian cell types and is typically protective; however, chronic activation contributes to pathologies including cancer and neurodegeneration. Canonical ISR (c-ISR) is initiated by phosphorylation of eIF2α in response to stressors such as endoplasmic reticulum or mitochondrial dysfunction, hypoxia, nutrient deprivation, and infections. This modification suppresses global protein synthesis while promoting ATF4 translation through upstream open reading frames (uORFs) in its 5'UTR. Recently, an alternative pathway, split ISR (s-ISR), enabling ATF4 translation independently of eIF2α phosphorylation, was identified in mice, suggesting ISR adaptability, though its relevance in humans remains unclear. Under normal conditions, cap-dependent translation predominates, mediated by the eIF4F complex and requiring the activity of eIF2B at its initial steps. During translational stress, eIF2α phosphorylation inhibits eIF2B activity, resulting in the formation of stalled initiation complexes, which can aggregate into stress granules (SGs). SGs sequester mRNAs and translation initiation factors, further repressing global translation, while ATF4 mRNA largely escapes sequestration, enabling selective translation. This partitioning highlights a finely tuned regulatory mechanism balancing ATF4 expression during stress. Recent advances reveal that, beyond cis-regulatory uORFs, trans-acting factors such as translation initiation factors and associated RNA-binding proteins critically influence ATF4 translation. Understanding these mechanisms provides insight into ISR plasticity and its implications for development, aging, and disease.
    Keywords:  ATF4 mRNA; RNA demethylases; RNA-binding proteins; eIFs; integrated stress response; stress granules; translation regulation; uORFs
    DOI:  https://doi.org/10.3390/cells15020188
  3. Plant Commun. 2026 Jan 23. pii: S2590-3462(26)00047-7. [Epub ahead of print] 101739
      Plant peptides have emerged as key regulators of plant growth, development, immunity, and environmental adaptation. Earlier studies in crops have demonstrated the potential application of certain peptides, such as systemin and Plant Elicitor Peptides (PEPs), to improve disease resistance. Based on the structure and function, these peptides are typically classified as canonical peptides (CPs), non-canonical peptides (NCPs), and non-ribosomal peptides (NRPs). Advances in peptidogenomics and mass spectrometry have enabled the genome-wide discovery of numerous endogenous peptides, including those translated from untranslated regions (UTRs) and non-coding RNAs, greatly expanding the plant peptidome. This review provides a comprehensive overview of the peptides, their classification, biosynthesis, and functional mechanisms in regulating various biological processes. Importantly, this review systematically summarizes the historical development and recent advances in strategies used to identify plant peptides. Despite substantial progress, peptide discovery and functional annotation remain challenging. Therefore, we finally propose that high-throughput technologies, functional genomics, and synthetic biology need to be integrated to reveal the potential of plant peptides in crop improvement and cross-disciplinary innovation.
    Keywords:  cross-disciplinary innovation; non-canonical peptides; peptidogenomics; plant peptides; receptor–ligand signaling
    DOI:  https://doi.org/10.1016/j.xplc.2026.101739
  4. Microlife. 2026 ;7 uqag002
      Quantitative information on protein abundance is crucial to understand biological processes and is therefore frequently gathered in proteomic studies. However, the quality of a quantitative proteomic dataset is greatly affected by the number of missing values, which need to be minimized to produce robust and meaningful data. In this context, small proteins (≤100 amino acids) pose specific analytical challenges, which hinder their efficient identification and quantitative characterization in complex proteomes. In this study, methods for sample preparation and MS-data processing are systematically evaluated for their contribution to identification and quantification of small proteins of Clostridioides difficile 630 Δerm. Results show that small protein enrichment can enhance the number of identified and quantified proteins also for low abundant small proteins. Through application of spectral libraries for identification of MS spectra the number of robustly quantified proteins is increased and a lower limit of their detection is reached. Additionally, the dataset presented here is currently the most comprehensive protein repository for C. difficile covering 84.7% of the predicted proteome and 61.4% of all predicted small proteins of this important pathogen.
    Keywords:  Clostridioides difficile; SEPs; database search; low molecular weight proteome; mass spectrometry; peptidomics; sProteins; spectral library
    DOI:  https://doi.org/10.1093/femsml/uqag002
  5. Cell. 2026 Jan 27. pii: S0092-8674(25)01437-0. [Epub ahead of print]
      Higher organisms spread external stimuli from the perceptive tissues to the whole body to achieve systemic responses. In plants, guard cells sense pathogens and close stomata to prevent their entry. We observed that pathogen-infected local leaves transmit the danger status to uninfected distal systemic leaves and trigger their stomatal closure as a global defense termed systemic stomatal immunity (SSIM). The underlying mobile signals remain unknown. Here, we report that an upstream open reading frame (uORF)-encoded systemic stomatal immune conductor (USIC) acts as a long-distance mobile peptide inducing SSIM. In local leaves, USIC increases upon pathogen/pattern signals and is secreted into the apoplast for long-distance transport. In systemic leaves, USIC is perceived by the cell surface SUCROSE-INDUCED RECEPTOR KINASE 1 (SIRK1)-KINASE 7 (KIN7) receptor complex and induces METACASPASE 4 (MC4)-mediated KIN7 cleavage. KIN7 associates with proton pumps/aquaporins to regulate stomatal closure. This study reveals a systemic signaling mechanism whereby an uORF-encoded mobile signal and its receptor pathway activate SSIM.
    Keywords:  KIN7; MC4; SIRK1; mobile peptide; receptor; systemic stomatal immunity; uORF
    DOI:  https://doi.org/10.1016/j.cell.2025.12.024
  6. Curr Protein Pept Sci. 2026 Jan 22.
       INTRODUCTION: The pathogenesis of age-related hearing loss (ARHL), especially the role of long non-coding RNAs (lncRNAs) and their encoded peptides, remains incompletely understood. This study aimed to characterize expression changes in lncRNAs and peptides in the cochleae of ARHL mice and explore the potential functions of lncRNA-encoded peptides via multi- -omics analysis.
    METHODS: C57BL/6J mice were used to establish the ARHL model. The molecular expression profiles of cochlear tissues from normal and ARHL mice were synthesized by lncRNA sequencing, peptidomics, and bioinformatics.
    RESULTS: Compared with the control group, a total of 789 differentially expressed lncRNAs and 466 differentially expressed peptides were identified in the ARHL group. Functional enrichment analysis revealed their association with key pathways, including ion transport, calcium signaling, the TCA cycle, and cytoskeleton regulation, indicating broad molecular dysregulation in the aging cochlea. Notably, 64 differentially expressed lncRNAs showed high translational potential, yielding 107 novel lncRNA-encoded peptides. These were mainly short peptides, some with stabilizing hydrophobic properties suited for membrane interactions, and enriched in domains like Pkinase and C2, suggesting involvement in signal transduction.
    DISCUSSION: These results emphasized that lncRNA-encoded peptides were novel regulators of ARHL, potentially regulating calcium homeostasis and mitochondrial function. The overlap of pathways such as the cytoskeleton and fatty acid metabolism indicated that the lncRNA-peptide axis drove auditory decline, providing institutional insights into the epigenetic basis of ARHL.
    CONCLUSION: Our findings suggest that lncRNA-encoded peptides are a novel class of regulatory molecules involved in the complex pathogenesis of ARHL, highlighting them as promising targets for future therapeutic strategies.
    Keywords:  Age-related hearing loss; bioinformatics; functional domain.; lncRNA-encoded peptides; long non-coding RNA; peptidomics
    DOI:  https://doi.org/10.2174/0113892037423330251019171447
  7. Front Genet. 2025 ;16 1756452
      Glioblastoma (GBM) remains a challenging tumour to mechanistically dissect, in part because of its capacity to adapt to hypoxia, metabolic imbalance and therapeutic pressure. Across cancer biology more broadly, attention has increasingly turned to ribosomal proteins (RPs). Although long regarded as stable structural components of the ribosome, several RPs show variation across tumour regions, stress states and differentiation trajectories. In some cancers, specific RPs have been mechanistically linked to selective translation or cell-state transitions, whereas in others the evidence remains largely associative. Overall, current observations leave open the question of whether RP variation reflects active regulatory roles or instead mirrors the broader physiological pressures experienced by malignant cells. In this mini review, we summarise what multi-omics approaches-including transcriptomics, proteomics and translatomics-currently reveal about RP regulation in GBM. Rather than making firm causal claims, we outline the main interpretations proposed so far, the uncertainties that complicate them and the conceptual gaps that keep the field open. Our aim is to provide a balanced and cautious overview that may help frame future work on how ribosomal components and the translational machinery could contribute to GBM plasticity.
    Keywords:  glioblastoma; multi-omics; ribosomal proteins; ribosome biogenesis; ribosome heterogeneity; translational regulation; tumour plasticity
    DOI:  https://doi.org/10.3389/fgene.2025.1756452