The various degrees of preharvest sprouting occurring in hybrid rice is a limiting factor in the propagation and production of hybrid rice seeds. The phenotype of sprouted rice is very similar to that of the maize (Zea mays) seed-specific mutation viviparous 1. VP1 has been shown to be a transcription factor essential for seed maturation and dormancy induction. In this study, numerous truncated transcripts of OsVP1 resulting from an unusual post-transcriptional processing, were detected in four rice (Oryza sativa) cultivars. The observed events took place at a region spanning exons 1 to 5, and led to a variety of deletions that resulted in the loss of functional domain and frame-shifts with premature termination by introducing a stop codon. Various proportions of the transcripts expressed in both immature and mature embryos were observed to be incorrectly processed and associated with the genetic variation of preharvest sprouting rates among various rice varieties. In sprouting-susceptible rice cultivars, G46B and HeiB, many more incorrectly processed OsVP1 transcripts were expressed in immature than in mature embryos, indicating that the unusual post-transcriptional processing of the OsVP1 gene was developmentally regulated. In addition, comprehensive sequence analyses demonstrated the presence of paired short direct repeats (SDRs) at the junctions of the unusual excision sites in exons of OsVP1 gene. Site selection for the deletion of exon materials was altered along with the genotypes and developmental stages.

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To analyze the genetic background of ‘white’ type Northern snakehead ( Channa argus ), and provide atheoretical basis for breeding of C. argus , the investigation of genetic diversity and population structure were investigated based on the complete sequences of mitochondrial DNA D-loop region for three cultured ‘white’ type C. argus populations, and four ‘bicolor’ type C. argus populations were used to compare with them; 28 mutation loci and 30 haplotypes were found in the D-loop sequence of all individuals with a total length of 907 bp. The highest haplotype diversity ( H d ) and nucleotide diversity ( P i ) in the ‘white’ type C. argus populations were 0.505 and 0.00057, respectively, which lower than those in the ‘bicolor’ type C. argus populations ( H d = 0.911, P i = 0.00326). Population differentiation values ( F ST ) show that the four ‘bicolor’ type C. argus populations had obvious genetic differentiation ( Fst : 0.21902–0.49428. p < 0.01), but not in the three ‘white’ type C. argus populations ( Fst : −0.00571 to 0.07261. p > 0.05). The phylogenetic tree and Median Joining (MJ) network showed that the genetic distance among ‘white’ type C. argus populations is very close. Therefore, much attention should be paid to protecting population genetic diversity and avoiding inbreeding in the breeding of ‘white’ type C. argus .

Background Lung cancer is a high incidence cancer on a worldwide basis and has become a major public health problem. Lung adenocarcinoma (LUAD) makes up approximately half of all lung cancers and is a threat to human health. Long non-coding RNAs (lncRNAs) is an important regulator of the development and progression of lung adenocarcinoma. In this manuscript we examined the role and potential mechanism of lncRNA PCAT6 in the development of LUAD. Methods and results Differences in lncRNA PCAT6 levels between LUAD samples and normal samples were first explored in the GEPIA database. We found that lncRNA PCAT6 expression was elevated, which was also validated in lung adenocarcinoma tissues and cell lines. Using western blotting, CCK-8, EdU, wound healing and transwell assays, we found that knockdown of lncRNA PCAT6 inhibited EMT, proliferation, migration, and invasion of LUAD cells. We noted a predicted a binding site for lncRNA PCAT6 and miR-545-3p through conducting bioinformatic analyses, and their binding was subsequently verified by a dual-luciferase reporter assay. Rescue experiments confirmed that miR-545-3p inhibitor partially abolished the inhibition function of lncRNA PCAT6 knockdown on LUAD cells. In addition, we predicted the downstream target genes of miR-545-3p and verified them by RT-qPCR. We found that EGFR was reduced in the silence of lncRNA PCAT6 and upregulated after miR-545-3p inhibition. Conclusion This study demonstrates that lncRNA PCAT6 promotes a more aggressive LUAD phenotype by sponging miR-545-3p. This finding may provide new ideas for the treatment of lung cancer.