Project description:Sugarcane streak mosaic virus (SCSMV) is the most important cause of sugarcane mosaic disease in the main production region. The SCSMV-encoded protein 1 (P1SCSMV) plays a vital role in disease development. However, the molecular mechanisms by which P1SCSMV participates in plant immunity remains unknown. Here, we found that the relative expression levels of P1SCSMV were negatively correlated with the xyloglucan endotransglucosylase/hydrolase gene (XTH) in a linear relationship. P1SCSMV directly interacts with the transcription factor, NbBES1, in vivo and in vitro. P1SCSMV-NbBES1 interaction interferes the binding of NbBES1 to the E-box element on the promoter region of NbXTH1 gene and inhibits the normal transcription of NbXTH1 gene. Furthermore, we found that down-regulation of the NbXTH1 directly resulted in enhanced infection of different plant pathogenic fungi and viruses, disrupted compositions of xyloglucan and xylan in the cell wall, and thinner middle lamellae in cell walls. We found that xyloglucan is a direct trigger of damage-associated molecular pattern- (DAMP) induced plant innate immunity. Moreover, the decrease in xyloglucan content in the cell wall caused by down-regulation of NbXTH1 leads to a reduction in DAMP-triggered immunity. Our study revealed the molecular mechanism of how a plant virus manipulates plant cell wall-mediated plant innate immunity, and identified NbXTH1, a wide-spectrum disease resistance protein for both plant pathogenic fungi and viruses. Our research also provides the basis for the application of the small molecule xyloglucan and the wide-spectrum disease resistance gene, XTH, in wide-spectrum resistance improvement in the future crop molecular breeding.
Project description:The molecular mechanisms underlying the development and progression of sugarcane mosaic virus (SCMV) infection in maize are poorly understood. A transcript profiling study based on maize unigene-microarrays was conducted to identify genes associated with SCMV resistance in the near isogenic line (NIL) pair F7+ (SCMV resistant) and F7 (susceptible). Four comparisons were conducted, which is addressing constitutive genetic discrepancy (Non-infected F7 vs. Non-infected F7+), inducible genetic discrepancy (Infected F7 vs. Infected F7+), compatible reaction (Non-infected F7 vs. Infected F7), and incompatible reaction (Non-infected F7+ vs. Infected F7+).
Project description:Wheat streak mosaic virus (WSMV) and Triticum mosaic virus (TriMV) are type members of Tritimovirus and Poacevirus genera, respectively, in the family Potyviridae, and are transmitted by wheat curl mites. Co-infection of these two viruses causes synergistic interaction with increased virus accumulation and disease severity in wheat. In this study, we examined the effects of synergistic interaction between WSMV and TriMV on endogenous small (s) RNAs and virus-specific small interfering RNAs (vsiRNAs) in susceptible (Arapahoe) and temperature-sensitive resistant (Mace) wheat cultivars at 27C and 18C. Single- and double-infections in wheat caused a shift in the profile of endogenous sRNAs from 24 nt being the most predominant in healthy plants to 21 nt in infected wheat. Additionally, we report high-resolution vsiRNA maps of WSMV and TriMV in singly- and doubly-infected wheat cultivars Arapahoe and Mace at 18C and 27C. Massive amounts of 21 and 22 nt vsiRNA reads were accumulated in Arapahoe at both temperatures and in Mace at 27C but not at 18C. The plus- and minus-sense vsiRNAs were distributed throughout the genomic RNAs in Arapahoe at both temperature regimens and in Mace at 27C, although some regions of genomic RNAs serve as hot-spots with an excessive number of vsiRNAs. The positions of vsiRNA peaks were conserved among wheat cultivars Arapahoe and Mace, suggesting that Dicer-like enzymes of susceptible and resistant wheat cultivars are similarly accessed the genomic RNAs of WSMV and TriMV. Additionally, several cold-spot regions were found in the genomes of TriMV and WSMV with no or a few vsiRNAs, indicating that certain regions of WSMV and TriMV genomes are not accessible to Dicer-like enzymes. The high-resolution map of endogenous and vsiRNAs from wheat cultivars synergistically infected with WSMV and TriMV at two temperature regimens form a foundation for understanding the virus-host interactions, effect of synergistic interactions on host defense mechanisms, and virus resistance mechanisms in wheat. Small RNA was sequenced from two wheat cultivars (Mace and Araphahoe), at two temperatures 18C and 27C, for healthy (control/uninfected), infected with wheat streak mosaic virus (WSMV), infected with Triticum mosaic virus (TriMV), and a double-infecttion of WSMV and TriMV.
Project description:Chinese soybean (Glycine max (L.) Merr.) cultivars Rsmv1 and Ssmv1 were used for soybean mosaic virus (SMV) resistance genes screening. The Rsmv1 cultivar was highly-resistant to SMV but the Ssmv1 cultivar was highly-susceptible. We used microarrays to detail the global programme of gene expression underlying SMV inoculation and identified distinct expression genes between Rsmv1 and Ssmv1.
Project description:Wheat streak mosaic virus (WSMV) and Triticum mosaic virus (TriMV) are type members of Tritimovirus and Poacevirus genera, respectively, in the family Potyviridae, and are transmitted by wheat curl mites. Co-infection of these two viruses causes synergistic interaction with increased virus accumulation and disease severity in wheat. In this study, we examined the effects of synergistic interaction between WSMV and TriMV on endogenous small (s) RNAs and virus-specific small interfering RNAs (vsiRNAs) in susceptible (Arapahoe) and temperature-sensitive resistant (Mace) wheat cultivars at 27ºC and 18ºC. Single- and double-infections in wheat caused a shift in the profile of endogenous sRNAs from 24 nt being the most predominant in healthy plants to 21 nt in infected wheat. Additionally, we report high-resolution vsiRNA maps of WSMV and TriMV in singly- and doubly-infected wheat cultivars Arapahoe and Mace at 18ºC and 27ºC. Massive amounts of 21 and 22 nt vsiRNA reads were accumulated in Arapahoe at both temperatures and in Mace at 27ºC but not at 18ºC. The plus- and minus-sense vsiRNAs were distributed throughout the genomic RNAs in Arapahoe at both temperature regimens and in Mace at 27ºC, although some regions of genomic RNAs serve as hot-spots with an excessive number of vsiRNAs. The positions of vsiRNA peaks were conserved among wheat cultivars Arapahoe and Mace, suggesting that Dicer-like enzymes of susceptible and resistant wheat cultivars are similarly accessed the genomic RNAs of WSMV and TriMV. Additionally, several cold-spot regions were found in the genomes of TriMV and WSMV with no or a few vsiRNAs, indicating that certain regions of WSMV and TriMV genomes are not accessible to Dicer-like enzymes. The high-resolution map of endogenous and vsiRNAs from wheat cultivars synergistically infected with WSMV and TriMV at two temperature regimens form a foundation for understanding the virus-host interactions, effect of synergistic interactions on host defense mechanisms, and virus resistance mechanisms in wheat.