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1.
Sci Rep ; 13(1): 3647, 2023 03 04.
Artículo en Inglés | MEDLINE | ID: mdl-36871121

RESUMEN

RNA interference is a highly conserved mechanism wherein several types of non-coding small RNAs regulate gene expression at the transcriptional or post-transcriptional level, modulating plant growth, development, antiviral defence, and stress responses. Argonaute (AGO), DCL (Dicer-like), and RNA-dependent RNA polymerase (RDR) are key proteins in this process. Here, these three protein families were identified in Chenopodium quinoa. Further, their phylogenetic relationships with Arabidopsis, their domains, three-dimensional structure modelling, subcellular localization, and functional annotation and expression were analysed. Whole-genome sequence analysis predicted 21 CqAGO, eight CqDCL, and 11 CqRDR genes in quinoa. All three protein families clustered into phylogenetic clades corresponding to those of Arabidopsis, including three AGO clades, four DCL clades, and four RDR clades, suggesting evolutionary conservation. Domain and protein structure analyses of the three gene families showed almost complete homogeneity among members of the same group. Gene ontology annotation revealed that the predicted gene families might be directly involved in RNAi and other important pathways. Largely, these gene families showed significant tissue-specific expression patterns, RNA-sequencing (RNA-seq) data revealed that 20 CqAGO, seven CqDCL, and ten CqRDR genes tended to have preferential expression in inflorescences. Most of them being downregulated in response to drought, cold, salt and low phosphate stress. To our knowledge, this is the first study to elucidate these key protein families involved in the RNAi pathway in quinoa, which are significant for understanding the mechanisms underlying stress responses in this plant.


Asunto(s)
Arabidopsis , Chenopodium quinoa , Filogenia , Antivirales , Proteínas Argonautas
2.
Arch Microbiol ; 202(1): 161-169, 2020 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-31549206

RESUMEN

Many kinds of antibiotics have effects on intestinal structure and function. In the current experimental study, we evaluate the effect of oral florfenicol on intestinal barrier in mice. Thirty adult male mice were randomly divided into two groups, the group none (N) and the group florfenicol (F), the mice in group F were orally administered florfenicol 100 mg/kg body weight (BW) for 7 days. At day 8, mice were euthanized and sampled for the analysis of alterations in genes and proteins from jejunum, jejunum morphology and microbiota analysis. Administration of florfenicol caused higher liver index (P < 0.05). In the jejunum, mucosa injury and villus rupture, compared with the group N, the villus length and V/C (villus length/crypt depth) in group F were marked decrease (P < 0.01). The transcription level of Muc2 and occludin in group F were significantly lower than those in group N (P < 0.01 or P < 0.05). The expression of APRIL, IL-17, IL-22, BAFF and sIgA on protein level were significantly down-regulated (P < 0.01 or P < 0.05), while the expression of IL-10, TGF-ß, IL-6, IL-4 were significantly up-regulated (P < 0.01) in group F. The abundances of bacteria in Firmicutes and Lactobacillus decreased significantly (P < 0.01) in group F. Our results indicated that oral administration of florfenicol might have a negative impact on functions of intestinal mucosal barrier, immune system and the intestinal microbiota.


Asunto(s)
Microbioma Gastrointestinal/efectos de los fármacos , Mucosa Intestinal/efectos de los fármacos , Tianfenicol/análogos & derivados , Administración Oral , Animales , Antibacterianos/administración & dosificación , Antibacterianos/efectos adversos , Antibacterianos/farmacología , Firmicutes/efectos de los fármacos , Regulación de la Expresión Génica/efectos de los fármacos , Interleucina-10 , Yeyuno/efectos de los fármacos , Lactobacillus/efectos de los fármacos , Masculino , Ratones , Distribución Aleatoria , Tianfenicol/administración & dosificación , Tianfenicol/efectos adversos , Tianfenicol/farmacología
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