Photosynthesis occurs mainly in chloroplasts, whose development is regulated by proteins encoded by nuclear genes.  Among them, pentapeptide repeat (PPR) proteins participate in organelle RNA editing.  Although there are more than 450 members of the PPR protein family in rice, only a few affect RNA editing in rice chloroplasts.  Gene editing technology has created new rice germplasm and mutants, which could be used for rice breeding and gene function study.  This study evaluated the functions of OsPPR9 in chloroplast RNA editing in rice.  The osppr9 mutants were obtained by CRISPR/Cas9, which showed yellowing leaves and a lethal phenotype, with suppressed expression of genes associated with chloroplast development and accumulation of photosynthetic-related proteins.  In addition, loss of OsPPR9 protein function reduces the editing efficiency of rps8-C182, rpoC2-C4106, rps14-C80, and ndhB-C611 RNA editing sites, which affects chloroplast growth and development in rice.  Our data showed that OsPPR9 is highly expressed in rice leaves and encodes a DYW-PPR protein localized in chloroplasts.  Besides, the OsPPR9 protein was shown to interact with OsMORF2 and OsMORF9.  Together, our findings provide insights into the role of the PPR protein in regulating chloroplast development in rice. 

Mycotoxins are the most widely present pollutants in both dietary provisions and livestock feed, and they pose a series of hazards for humans and animals. Deoxynivalenol (DON) is a prevalent mycotoxin that is primarily produced by Fusarium spp. and commonly found in various cereal products. Feeding swine diets contaminated with trichothecene DON can lead to major adverse effects, including reduced feed intake, diminished weight gains, and compromised immune function. Among all animal species tested, swine were the most sensitive to DON. Here we explored the disruption of gut health by DON, considering aspects such as intestinal histomorphology, epithelial barrier functions, the intestinal immune system, microflora, and short-chain fatty acid production in the intestines. Numerous additives have been documented for their potential in the detoxification of DON. These additives can alleviate the toxic effects of DON on pigs by modulating the Nrf2-Keap1, mitogen-activated protein kinases (MAPKs) and Nuclear factor kappa-B (NF-κB) signaling pathways. Additionally, there are additives capable of mitigating the toxicity of DON through adsorption or biotransformation. This update has novel potential for advancing our comprehension of the mechanisms linked to DON intestinal toxicity and facilitating the formulation of innovative strategies to mitigate the impact of DON.