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N6-methyladenosine (m6A), the most abundant and common modification on eukaryotic mRNA, plays crucial roles in multiple biological processes through controlling endogenous gene activity in organisms. The m6A reader specifically recognizes the m6A mark to mediate the regulation of m6A on mRNA, and determines the fate of its target mRNA. In plants, the currently confirmed m6A readers are YTH (YT521B homology) domain-containing proteins. We previously reported that tomato contains 9 YTH genes, of which SlYTH1 has the strongest expression. The present study reports the functional characterization of SlYTH1 in tomato. SlYTH1 mutants generated via CRISPR/Cas9 technology exhibited pleiotropic phenotypes, including low seed germination rate, shortened seedling root, retarded plant growth and development during vegetative development, and elongated and longitudinally flattened fruit with reduced the locule number. SlYTH1 knockout reduced GA 3 content and downregulated the expression of related genes in gibberellin biosynthesis pathway. Moreover, exogenous GA 3 application could partially restore the phenotypic defects caused by SlYTH1 mutations. SlYTH1 knockout could alleviate the inhibition of seedling root elongation by exogenous GA 3 application at relatively low concentration. These facts indicated SlYTH1 is involved in regulating gibberellin biosynthesis and plays important roles in multiple physiological processes in tomato. • Tomato SlYTH1 knockout reduced seed germination rate, and retarded plant vegetative development. • SlYTH1 mutations produced elongated and longitudinally flattened fruit with reduced the locule number. • SlYTH1 mutations reduced GA 3 content, and exogenous GA 3 could partially rescue the phenotypic defects of SlYTH1 mutants. [ABSTRACT FROM AUTHOR]

Severe trauma can lead to numerous serious complications, threating the well-being and vitality of the afflicted. The quantity and functionality of PMNs undergo rapid transformations in response to severe trauma, playing a pivotal role in the trauma response. The absence of CCAAT/enhancer-binding protein ε (C/EBPε) profoundly impairs the functionality of polymorphonuclear neutrophils (PMNs), a function of paramount importance in trauma. In this study, by generating mice with C/EBPε knocked out or overexpressed, we substantiate that C/EBPε ensures the restoration of PMN function, enhancing the expression of antimicrobial proteins and thereby promoting trauma recovery. Furthermore, diminished expression of C/EBPε is observed in trauma patients, with levels displaying a negative correlation with ISS and APACHE II scores, suggesting its potential as a prognostic indicator for clinical treatment. Mechanistically, we uncover the upregulation of SIRT1 and the inhibition of P300 participating in the suppression of C/EBPε acetylation, consequently reducing the resilience of mice to trauma. As therapeutic interventions, whether through the sole administration of PMN, NAM treatment, or their combination, all result in an increased survival rate in traumatic mice. In conclusion, our study elucidates the role of C/EBPε in enhancing the resilience to trauma and identifies C/EBPε acetylation as a critical regulatory mechanism, offering potential therapeutic approaches involving PMN transfusion and NAM treatment., (© The Author(s) 2024. Published by Oxford University Press on behalf of the British Society for Immunology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)