Effect of ethylene production by four pathogenic fungi on the postharvest diseases of green pepper (Capsicum annuum L.).

Ethylene produced by plants generally induces ripening and promotes decay, whereas the effect of ethylene produced by pathogens on plant diseases remains unclear. In this study, four ethylene-producing fungi including Alternaria alternata (A. alternata, Aa), Fusarium verticilliodes (F. verticillioides, Fv), Fusarium fujikuroi 1 (F. fujikuroi 1, Ff-1) and Fusarium fujikuroi 2 (F. fujikuroi 2, Ff-2) were severally inoculated in potato dextrose broth (PDB) media and postharvest green peppers, the ethylene production rates, disease indexes and chlorophyll fluorescence parameters were determined. The results showed that Ff-2 and Fv in the PDB media had the highest and almost the same ethylene production rates. After inoculation with green peppers, Ff-2 treated group still exhibited the highest ethylene production rate, whereas Aa treated group had a weak promotion effect on ethylene production. Moreover, the ethylene production rate of green peppers with mechanical injury was twice that without mechanical injury, and the ethylene production rates of green peppers treated with Aa, Ff-1, Ff-2 and Fv were 1.2, 2.6, 3.8 and 2.8 folds than those of green peppers without treatment, respectively. These results indicated that pathogen infection stimulated the synthesis of ethylene in green peppers. Correlation analysis indicated that the degreening of Fusarium-infected green pepper was significantly positively correlated with the ethylene production rate of green pepper, whereas the disease spot of Aa-infected green pepper had a significant positive correlations with the ethylene production rate of green peppers. Chlorophyll fluorescence results showed that the green peppers already suffered from severe disease after being infected with fungi for 4 days, and Fusarium infection caused early and serious stress, while the harm caused by A. alternata was relatively mild at the early stage. Our results clearly showed that α-keto-γ-methylthiobutyric acid (KMBA)-mediated ethylene synthesis was the major ethylene synthesis pathway in the four postharvest pathogenic fungi. All the results obtained suggested that ethylene might be the main infection factor of Fusarium spp. in green peppers. For pathogenic fungi, stimulating green peppers to produce high level of ethylene played a key role in the degreening of green peppers.

The m6A reader YTHDC2 maintains visual function and retinal photoreceptor survival through modulating translation of PPEF2 and PDE6B.

Inherited retinal dystrophies (IRDs) are major causes of visual impairment and irreversible blindness worldwide, while the precise molecular and genetic mechanisms are still elusive. N6-methyladenosine (m6A) modification is the most prevalent internal modification in eukaryotic mRNA. YTH domain containing 2 (YTHDC2), an m6A reader protein, has recently been identified as a key player in germline development and human cancer. However, its contribution to retinal function remains unknown. Here, we explore the role of YTHDC2 in the visual function of retinal rod photoreceptors by generating rod-specific Ythdc2 knockout mice. Results show that Ythdc2 deficiency in rods causes diminished scotopic ERG responses and progressive retinal degeneration. Multi-omics analysis further identifies Ppef2 and Pde6b as the potential targets of YTHDC2 in the retina. Specifically, via its YTH domain, YTHDC2 recognizes and binds m6A-modified Ppef2 mRNA at the coding sequence and Pde6b mRNA at the 5'-UTR, resulting in enhanced translation efficiency without affecting mRNA levels. Compromised translation efficiency of Ppef2 and Pde6b after YTHDC2 depletion ultimately leads to decreased protein levels in the retina, impaired retinal function, and progressive rod death. Collectively, our finding highlights the importance of YTHDC2 in visual function and photoreceptor survival, which provides an unreported elucidation of IRD pathogenesis via epitranscriptomics.

Regulation of hepatic gluconeogenesis by nuclear factor Y transcription factor in mice.

Hepatic gluconeogenesis is essential to maintain blood glucose levels, and its abnormal activation leads to hyperglycemia and type 2 diabetes. However, the molecular mechanisms in the regulation of hepatic gluconeogenesis remain to be fully defined. In this study, using murine hepatocytes and a liver-specific knockout mouse model, we explored the physiological role of nuclear factor Y (NF-Y) in regulating hepatic glucose metabolism and the underlying mechanism. We found that NF-Y targets the gluconeogenesis pathway in the liver. Hepatic NF-Y expression was effectively induced by cAMP, glucagon, and fasting in vivo Lentivirus-mediated NF-Y overexpression in Hepa1-6 hepatocytes markedly raised the gluconeogenic gene expression and cellular glucose production compared with empty vector control cells. Conversely, CRISPR/Cas9-mediated knockdown of NF-Y subunit A (NF-YA) attenuated gluconeogenic gene expression and glucose production. We also provide evidence indicating that CRE-loxP-mediated, liver-specific NF-YA knockout compromises hepatic glucose production. Mechanistically, luciferase reporter gene assays and ChIP analysis indicated that NF-Y activates transcription of the gluconeogenic genes Pck1 and G6pc, by encoding phosphoenolpyruvate carboxykinase (PEPCK) and the glucose-6-phosphatase catalytic subunit (G6Pase), respectively, via directly binding to the CCAAT regulatory sequence motif in their promoters. Of note, NF-Y enhanced gluconeogenesis by interacting with cAMP-responsive element-binding protein (CREB). Overall, our results reveal a previously unrecognized physiological function of NF-Y in controlling glucose metabolism by up-regulating the gluconeogenic genes Pck1 and G6pc Modulation of hepatic NF-Y expression may therefore offer an attractive therapeutic approach to manage type 2 diabetes.