RESUMEN
Salt marsh plants play a vital role in mediating nitrogen (N) biogeochemical cycle in estuarine and coastal ecosystems. However, the effects of invasive Spartina alterniflora on N fixation and removal, as well as how these two processes balance to determine the N budget, remain unclear. Here, simultaneous quantifications of N fixation and removal via 15N tracing experiment with native Phragmites australis, invasive S. alterniflora, and bare flats as well as corresponding functional gene abundance by qPCR were carried out to explore the response of N dynamics to S. alterniflora invasion. Our results showed that N fixation and removal rates ranged from 0.77 ± 0.08 to 16.12 ± 1.13 nmol/(g·h) and from 1.42 ± 0.14 to 16.35 ± 1.10 nmol/(g·h), respectively, and invasive S. alterniflora generally facilitated the two processes rates. Based on the difference between N removal and fixation rates, net N2 fluxes were estimated in the range of -0.39 ± 0.14 to 8.24 ± 2.23 nmol/(g·h). Estimated net N2 fluxes in S. alterniflora stands were lower than those in bare flats and P. australis stands, indicating that the increase in N removal caused by S. alterniflora invasion may be more than offset by N fixation process. Random forest analysis revealed that functional microorganisms were the most important factor associated with the corresponding N transformation process. Overall, our results highlight the importance of N fixation in evaluating N budget of estuarine and coastal wetlands, providing valuable insights into the ecological effect of S. alterniflora invasion.
RESUMEN
Triclosan (TCS) and triclocarban (TCC) are two common antimicrobial compounds, which are widely used as ingredients in pharmaceuticals and personal care products. They occur ubiquitously in soil due to biosolid application as agricultural fertilizers, but their influence on microbially mediated soil biogeochemical processes is poorly understood. We tested the effects of varying concentrations of TCS and TCC applied both individually and together on denitrification and N2O emissions in paddy soil. We also quantified denitrification functional gene abundances by q-PCR to elucidate the microbial mechanisms of TCS and TCC's effects. Our results showed that TCS and TCC exposure both individually and together significantly (pâ¯<â¯0.05) inhibited denitrification (7.0-36.7%) and N2O emissions (15.4-86.4%) except for the 0.01â¯mgâ¯kg-1 TCC treatment in which denitrification was slightly but significantly (pâ¯<â¯0.05) stimulated. The inhibitory effects of TCS and TCC exposure were mainly attributed to their negative net effects on denitrifying bacteria as suggested by the decrease in abundances of 16S rRNA, narG, nirK and clade I nosZ genes in the TCS and TCC treatments. Overall, we found that TCS and TCC exposure in paddy soil could substantially alter nitrogen cycling in rice paddy ecosystems by inhibiting denitrification and N2O emissions. These effects should be taken into consideration when evaluating the environmental impacts of TCS and TCC.
RESUMEN
Puccinia striiformis f. sp. tritici (Pst), the causal agent of stripe rust, is an obligate biotrophic pathogen responsible for severe wheat disease epidemics worldwide. Pst and other rust fungi are acknowledged to deliver many effector proteins to the host, but little is known about the effectors' functions. Here, we report a candidate effector Pst_8713 isolated based on the genome data of CY32 and the expression of Pst_8713 is highly induced during the early infection stage. The Pst_8713 gene shows a low level of intra-species polymorphism. It has a functional N-terminal signal peptide and its product was found in the host cytoplasm and nucleus. Co-infiltrations in Nicotiana benthamiana demonsrated that Pst_8713 was capable of suppressing cell death triggered by mouse pro-apoptotic protein-BAX or Phytophthora infestans PAMP-INF1. Overexpression of Pst_8713 in plants suppressed pattern-triggered immunity (PTI) -associated callose deposition and expression of PTI-associated marker genes and promoted bacterial growth in planta. Effector-triggered immunity (ETI) induced by an avirulent Pst isolate was weakened when we overexpressed Pst_8713 in wheat leaves which accompanied by reduction of reactive oxygen species (ROS) accumulation and hypersensitive response (HR). In addition, the host induced gene silencing (HIGS) experiment showed that knockdown of Pst_8713 weakened the virulence of Pst by producing fewer uredinia. These results indicated that candidate effector Pst_8713 is involved in plant defense suppression and contributes to enhancing the Pst virulence.
RESUMEN
The actin cytoskeleton has been implicated in plant defense against pathogenic fungi, oomycetes, and bacteria. Actin depolymerizing factors (ADFs) are stimulus responsive actin cytoskeleton modulators. However, there is limited evidence linking ADFs with plant defense against pathogens. In this study, we have isolated and functionally characterized a stress-responsive ADF gene (TaADF3) from wheat, which was detectable in all examined wheat tissues. TaADF3 is a three-copy gene located on chromosomes 5AL, 5BL, and 5DL. A particle bombardment assay in onion epidermal cells revealed the cytoplasmic and nuclear localization of TaADF3. The expression of TaADF3 was inducible by abscisic acid (ABA), as well as various abiotic stresses (drought and cold) and virulent Puccinia striiformis f. sp. tritici (Pst) but was down regulated in response to avirulent Pst. Virus-induced silencing of TaADF3 copies enhanced wheat resistance to avirulent Pst, with decreased reactive oxygen species (ROS) accumulation and hypersensitive response (HR). Upon treatment with virulent Pst, TaADF3-knockdown plants exhibited reduced susceptibility, which was accompanied by increased ROS production and HR. Interestingly, the silencing of TaADF3 resulted in hindered pathogen penetration and haustoria formation for both avirulent and virulent Pst. Moreover, the array and distribution of actin filaments was transformed in TaADF3-knockdown epidermal cells, which possibly facilitated attenuating the fungus penetration. Thus, our findings suggest that TaADF3 positively regulates wheat tolerance to abiotic stresses and negatively regulates wheat resistance to Pst in an ROS-dependent manner, possibly underlying the mechanism of impeding fungal penetration dependent on the actin architecture dynamics.