The photosensory function of Zmphot1 differs from that of Atphot1 due to the C-terminus of Zmphot1 during phototropic response

The role of phot1 in triggering hypocotyl phototropism and optimizing growth orientation has been wellcharacterized in Arabidopsis, whereas the role of Zmphot1 in maize remains largely unclear. Here, we show that Zmphot1 is involved in blue light-induced phototropism. Compared with Atphot1, Zmphot1exhibited a weaker phototropic response to very low-fluence rates of blue light(< 0.01 μmol m-2s-1),but stronger phototropic response to high-fluence rates of blue light(> 10 μmol m-2s-1) than Atphot1. Notably, blue light exposure induced Zmphot1-green fluorescent protein(GFP), but not Atphot1-GFP, to form the aggregates in the cytoplasm of Nicotiana benthamiana cells. Furthermore, by generating the chimeric phot1 proteins, we found that the serine-threonine kinase(STK) domain at the C-terminus is responsible for a more volatile membrane association of Zmphot1. Consistently, the chimeric phot1 protein fusing the STK domain of Zmphot1 with other domains of Atphot1 responded similarly as Zmphot1 to both low and high fluence rates of blue light. Interestingly, although both Zmphot1 and Atphot1 interact with AtNPH3, Zmphot1 induced weaker dephosphorylation of NONPHOTOTROPIC HYPOCOTYL 3(NPH3) than Atphot1. Together, our findings indicate that Zmphot1 and Atphot1 exhibit different photosensory function during phototropic response and that the STK domain may play a key role in determining their properties.

Large-scale analysis of small RNAs derived from traditional Chinese herbs in human tissues

Plant-derived microRNAs have recently been reported to function in human blood and tissues. Controversy was immediately raised due to possible contamination and the lack of large sample sizes. Here, we report thousands of unique small RNAs derived from traditional Chinese medicine(TCM) herbs found in human blood cells and mouse lung tissues using a large-scale analysis.We extracted small RNAs from decoctions of 10 TCM plants(Ban Zhi Lian, Chai Hu, Chuan Xin Lian, Di Ding Zi Jin, Huang Qin, Jin Yin Hua, Lian Qiao, Pu Gong Ying, Xia Ku Cao, and Yu Xing Cao) and obtained millions of RNA sequences from each herb. We also obtained RNA-Seq data from the blood cells of humans who consumed herbal decoctions and from the lung tissues of mice administered RNAs from herbal decoctions via oral gavage. We identified thousands of unique small RNA sequences in human blood cells and mouse lung tissues. Some of these identified small RNAs from Chuan Xin Lian and Hong Jing Tian could be mapped to the genomes of the herbs, confirming their TCM plant origin. Small RNAs derived from herbs regulate mammalian gene expression in a sequence-specific manner, and thus are a superior novel class of herbal drug components that hold great potential as oral gene-targeted therapeutics, highlighting the important role of herbgenomics in their development.

Plant-derived phosphocholine facilitates cellular uptake of anti-pulmonary fibrotic HJT-sRNA-m7

Pulmonary fibrosis, a progressive chronic disease with a high mortality rate, has limited treatment options. Currently, lung transplantation remains the only effective treatment. Here we report that a small RNA, HJT-sRNA-m7, from a Chinese herbal medicine Hong Jing Tian(HJT, RHODIOHAE CRENULATAE RADIX ET RHIZOMA, Rhodiola crenulata) can effectively reduce the expressions of fibrotic hallmark genes and proteins both in alveolar in vitro and in mouse lung tissues in vivo. We also discovered over one hundred oil-soluble chemicals from HJT decoctions, most of which are found in lipid extracts from other Chinese herbals decoctions, including Pu Gong Ying(PGY, TARAXACI HERBA, Taraxacum mongolicum), Chuan Xin Lian(CXL, changed to "ANDROGRAPHIS HERBA, Andrographis paniculata"), and Jin Yin Hua(JYH, lonicera japonica or Honeysuckle). We identified the active component in these decoctions as two forms of phosphocholines, PC(18:0/18:2) and PC(16:0/18:2). These PCs potentially could form liposomes with small RNAs to enter human alveolar and gastric cells. Our experimental results suggest an unprecendent lipid complex route through which botanic small RNA can enter human bodies.Our results provide an innovative treatment strategy for oral delivery of siRNAs as therapeutic medication.

Tauroursodeoxycholic acid(TUDCA) inhibits influenza A viral infection by disrupting viral proton channel M2

Influenza is a persistent threat to human health and there is a continuing requirement for updating antiinfluenza strategies. Initiated by observations of different endoplasmic reticulum(ER) responses of host to seasonal H1N1 and highly pathogenic avian influenza(HPAI) A H5N1 infections, we identified an alternative antiviral role of tauroursodeoxycholic acid(TUDCA), a clinically available ER stress inhibitor, both in vitro and in vivo. Rather than modulating ER stress in host cells, TUDCA abolished the proton conductivity of viral M2 by disrupting its oligomeric states, which induces inefficient viral infection. We also showed that M2 penetrated cells, whose intracellular uptake depended on its proton channel activity,an effect observed in both TUDCA and M2 inhibitor amantadine. The identification and application of TUDCA as an inhibitor of M2 proton channel will expand our understanding of IAV biology and complement current anti-IAV arsenals.

Phot2-regulated relocation of NPH_3 mediates phototropic response to high-intensity blue light in Arabidopsis thaliana

Two redundant blue-light receptors, known as phototropins （phot1 and phot2）, influence a variety of physiological responses, including phototropism, chloroplast positioning, and stomatal opening in Arabidopsis thaliana. Whereas photl functions in both low- and high-intensity blue light （HBL）, phot2 functions primarily in HBL. Here, we aimed to elucidate phot2-specific functions by screening for HBL- insensitive mutants among mutagenized Arabidopsis photl mutants. One of the resulting phot2 signaling associated （p2sa） double mutants, phot1 p2sa2, exhibited phototropic defects that could be restored by constitutively expressing NON-PHOTOTROPIC HYPOCOTYL 3 （NPH3）, indicating that P2SA2 was allelic to NPH3. It was observed that NPH3-GFP signal mainly localized to and clustered on the plasma membrane in darkness. This NPH3 clustering on the plasmamembrane was not affected by mutations in genes encoding proteins that interact with N PH3, including PHOT11, PHOT2 and ROOTPHOTOTROPISM 2 （RPT2）. However, the HBL irradiation- mediated release of NPH3 proteins into the cytoplasm was inhibited in photl mutants and enhanced in phot2 and rpt2-2 mutants. Furthermore, HBL-induced hypocotyl phototropism was enhanced in photl mutants and inhibited in the phot2 and rpt2-2 mutants. Our findings indicate that photl regulates the dissociation of NPH3 from the plasma membrane, whereas phot2 mediates the stabilization and relocation of NPH3 to the plasma membrane to acclimate to HBL.

Corrigendum to"Tauroursodeoxycholic acid(TUDCA)inhibits influenza A viral infection by disrupting viral proton channel M2"[Sci.Bull.,64(3)(2019)180-188]

Following the published article[1].the authors noticed an error duplication of image of DAPI in Fig.2c"AF"and"No pretreated and without TUDCA".The correct DAPI image was in the merged image of"No pretreated and without TUDCA"of the published article.Therefore,the corrected Fig.2c should be as follows:The online version of the original artice can be found at https://doi.org/10.101/j.scib.2018.08.0131.