Genome-wide identification and expression analysis of the glycosyl hydrolase family 1 genes in Medicago sativa revealed their potential roles in response to multiple abiotic stresses.

Glycoside hydrolase family 1 (GH1) ß-glucosidases (BGLUs), are encoded by a large number of genes, which participate in the development and stress response of plants, particularly under biotic and abiotic stresses through the activation of phytohormones. However, there are few studies systematically analyzing stress or hormone-responsive BGLU genes in alfalfa. In this study, a total of 179 BGLU genes of the glycoside hydrolase family 1 were identified in the genome of alfalfa, and then were classified into five distinct clusters. Sequence alignments revealed several conserved and unique motifs among these MsBGLU proteins. Many cis-acting elements related to abiotic stresses and phytohormones were identified in the promoter of some MsBGLUs. Moreover, RNA-seq and RT-qPCR analyses showed that these MsBGLU genes exhibited distinct expression patterns in response to different abiotic stress and hormonal treatments. In summary, this study suggests that MsBGLU genes play crucial roles in response to various abiotic stresses and hormonal responses, and provides candidate genes for stress tolerance breeding in alfalfa.

Integrated physiological, metabolomic, and transcriptomic analyses elucidate the regulation mechanisms of lignin synthesis under osmotic stress in alfalfa leaf (Medicago sativa L.).

Alfalfa, an essential forage crop known for its high yield, nutritional value, and strong adaptability, has been widely cultivated worldwide. The yield and quality of alfalfa are frequently jeopardized due to environmental degradation. Lignin, a constituent of the cell wall, enhances plant resistance to abiotic stress, which often causes osmotic stress in plant cells. However, how lignin responds to osmotic stress in leaves remains unclear. This study explored the effects of osmotic stress on lignin accumulation and the contents of intermediate metabolites involved in lignin synthesis in alfalfa leaves. Osmotic stress caused an increase in lignin accumulation and the alteration of core enzyme activities and gene expression in the phenylpropanoid pathway. We identified five hub genes (CSE, CCR, CADa, CADb, and POD) and thirty edge genes (including WRKYs, MYBs, and UBPs) by integrating transcriptome and metabolome analyses. In addition, ABA and ethylene signaling induced by osmotic stress regulated lignin biosynthesis in a contradictory way. These findings contribute to a new theoretical foundation for the breeding of high-quality and resistant alfalfa varieties.

Zinc oxide nanoparticles derived from Penicillium griseofulvum mitigate DMBA/TPA-promoted mice skin carcinogenesis by modulating NF-ĸB associated signalling.

This study investigates the synthesis of zinc oxide nanoparticles using Penicillium griseofulvum (ZnONPs-PG) and their potential role in preventing DMBA/TPA-induced skin cancer. The synthesis process involved using a 1-mM zinc acetate dihydrate as a precursor in P. griseofulvum. Various analytical techniques, including FTIR spectroscopy, UV-Vis, TEM, XRD, and DLS, were utilized to characterize the ZnONPs. The efficacy of ZnONPs-PG was then evaluated in a DMBA/TPA-induced skin cancer model. Mice were treated topically with DMBA/TPA in acetone (200 µL) over 2 weeks, with treatments continuing for 20 weeks. Results showed 100% tumor occurrence, histological changes, elevated lipid peroxidation (LPO) levels, and decreased antioxidant levels in DMBA/TPA-treated mice. However, topical application of ZnONPs magnificently reverted the tumor occurrence, histological changes, elevated malanoldehyde and hydrogen peroxide levels; decreased antioxidant levels in DMBA/TPA-treated mice. ZnONPs-PG treatment suppressed the increased levels of inflammatory markers (COX-2, iNOS and NF-κB,) and cell proliferation markers (Cyclin-E1, Cyclin D1, VEGF, TGF-ß1) exposed mice. In addition, ZnONPs-PG treatment decreased the DMBA/TPA-induced anti-apoptotic Bcl-2 protein and increasing the expression of pro-apoptotic markers (Bax and caspase 3) in skin tissues. Thus, ZnONPs-PG may prevent skin carcinogenesis through its potent antioxidant properties and inhibiting NF-κB-mediated inflammatory and proliferation pathways.

NEDD4L represses prostate cancer cell proliferation via modulating PHF8 through the ubiquitin–proteasome pathway

Purpose Prostate cancer (PC) is a heterogeneous malignancy that greatly threatens man’s health. E3 ubiquitin-protein ligase neural precursor cell expressed developmentally downregulated 4-like (NEDD4L) imparts an regulatory role in various malignancies. This study focused on the modulatory mechanism of NEDD4L in proliferation of prostate cancer cells (PCCs) via regulating histone demethylase plant homeodomain finger protein 8 (PHF8/KDM7B) through the ubiquitin–proteasome system. Methods The expression levels of NEDD4L, PHF8, H3 lysine 9 dimethylation (H3K9me2) and activating transcription factor 2 (ATF2) in PC tissues and cell lines were detected via real-time quantitative polymerase chain reaction and Western blotting. After transfection of pcDNA3.1-NEDD4L, pcDNA3.1-PHF8, and pcDNA3.1-ATF2 into PCCs, cell proliferation was assessed via the cell counting kit-8 and 5-ethynyl-2'-deoxyuridine assays. Interaction between NEDD4L and PHF8 was identified via the protein immunoprecipitation. The ubiquitination level of PHF8 was determined via the ubiquitination detection. The enrichments of H3K9me2 and PHF8 in the ATF2 promotor region were detected via the chromatin-immunoprecipitation assay. Results PHF8 and ATF2 were highly expressed while NEDD4L was poorly expressed in PC tissues and cells. NEDD4L overexpression reduced proliferation of PCCs. NEDD4L induced degradation of PHF8 via ubiquitination. PHF8 limited the enrichment of H3K9me2 in the ATF2 promotor region and enhanced ATF2 transcription. Up regulation of PHF8 or ATF2 abolished the inhibitory role of NEDD4L in proliferation of PCCs. Conclusion NEDD4L facilitated degradation of PHF8 to limit ATF2 transcription, thereby suppressing proliferation of PCCs. (AU)