[Correlation analysis of quality,origin and phenotypic characters of Paris polyphylla var. yunnanensis].

In order to provide guidance for the protection and utilization of resources,quality control and breeding of improved varieties,we compared the main phenotypic characters and quality of wild and transplanted Paris polyphylla var. yunnanensis collected from different producing areas. Seven phenotypic characters of 33 samples of P. polyphylla var. yunnanensis collected from Yunnan,Guizhou and Sichuan were determined by conventional methods,and the principal component analysis and cluster analysis were used to analyze the diversity of the samples. The parissaponin( polyphyllin Ⅰ,Ⅱ,Ⅵ,Ⅶ) content of the samples were detected by HPLC,and analyzed by cluster analysis. Correlation analysis of the phenotypic characters and the parissaponin content was performed. There were significant differences in seven phenotypic characters between wild and transplanted samples of P. polyphylla var. yunnanensis from different habitats,with high phenotypic diversity and abundant genetic variation. The results of principal component analysis showed that leaf shape index was the main factor of morphological variation of P. polyphylla var. yunnanensis. Cluster analysis showed that the phenotypic characters of wild and transplanted P. polyphylla var. yunnanensis could not be completely separated. The content of saponins in wild and transplanted samples from different habitats was quite different. Saponins content of 93. 94% samples met the criterion of Chinese Pharmacopoeia 2015 edition,and the overall quality was relatively steady. The results of independent sample t-test showed that there was no significant difference of all the active ingredient between wild and transplanted samples,and it couldn't be used to distinguish between wild and transplanted samples. It is the same as the results of cluster analysis. The results of correlation analysis showed that the phenotypic traits of P. polyphylla var. yunnanensis were correlated with its medicine quality,and the total content of saponins was positively correlated with leaf length and leaf shape index( r = 0. 389,0. 441; P<0. 05). Yunnan,Guizhou and Sichuan are suitable for the growth of P. polyphylla var. yunnanensis. And the transplaned P. polyphylla var. yunnanensis can be used as the same as the wild ones completely. The results provide reference for the protection and selective breeding of P. polyphylla var. yunnanensis.

New persistent plant RNA virus carries mutations to weaken viral suppression of antiviral RNA interference.

Persistent plant viruses are widespread in natural ecosystems. However, little is known about why persistent infection with these viruses may cause little or no harm to their host. Here, we discovered a new polerovirus that persistently infected wild rice plants by deep sequencing and assembly of virus-derived small-interfering RNAs (siRNAs). The new virus was named Rice tiller inhibition virus 2 (RTIV2) based on the symptoms developed in cultivated rice varieties following Agrobacterium-mediated inoculation with an infectious RTIV2 clone. We showed that RTIV2 infection induced antiviral RNA interference (RNAi) in both the wild and cultivated rice plants as well as Nicotiana benthamiana. It is known that virulent virus infection in plants depends on effective suppression of antiviral RNAi by viral suppressors of RNAi (VSRs). Notably, the P0 protein of RTIV2 exhibited weak VSR activity and carries alanine substitutions of two amino acids broadly conserved among diverse poleroviruses. Mixed infection with umbraviruses enhanced RTIV2 accumulation and/or enabled its mechanical transmission in N. benthamiana. Moreover, replacing the alanine at either one or both positions of RTIV2 P0 enhanced the VSR activity in a co-infiltration assay, and RTIV2 mutants carrying the corresponding substitutions replicated to significantly higher levels in both rice and N. benthamiana plants. Together, our findings show that as a persistent plant virus, RTIV2 carries specific mutations in its VSR gene to weaken viral suppression of antiviral RNAi. Our work reveals a new strategy for persistent viruses to maintain long-term infection by weak suppression of the host defence response.