Seven races of Striga gesnerioides parasitic on cowpea, a major food and forage legume in sub-Saharan Africa, have been identified. Race-specific resistance of cowpea to Striga involves a coiled-coil nucleotide binding site leucine-rich repeat domain resistance protein encoded by the RSG3-301 gene. Knockdown of RSG3-301 expression by virus-induced gene silencing in the multirace-resistant cowpea cultivar B301 results in the failure of RSG3-301-silenced plants to mount a hypersensitive response and promotes parasite necrosis when challenged with Striga race SG3, whereas the resistance response to races SG2 and SG5 is unaltered. Our findings indicate that a gene-for-gene resistance mechanism is operating in these unique plant-plant associations.

A recent review concluded that earthworm presence increases CO 2 emissions by 33% but does not affect soil organic carbon stocks. However, the findings are controversial and raise new questions. Here we hypothesize that neither an increase in CO 2 emission nor in stabilized carbon would entirely reflect the earthworms' contribution to net carbon sequestration. We show how two widespread earthworm invaders affect net carbon sequestration through impacts on the balance of carbon mineralization and carbon stabilization. Earthworms accelerate carbon activation and induce unequal amplification of carbon stabilization compared with carbon mineralization, which generates an earthworm-mediated 'carbon trap'. We introduce the new concept of sequestration quotient to quantify the unequal processes. The patterns of CO 2 emission and net carbon sequestration are predictable by comparing sequestration quotient values between treatments with and without earthworms. This study clarifies an ecological mechanism by which earthworms may regulate the terrestrial carbon sink.

Following the first human infection with the influenza A (H10N8) virus in Nanchang, China in December 2013, we identified two additional patients on January 19 and February 9, 2014. The epidemiologic, clinical, and virological data from the patients and the environmental specimen collected from 23 local live poultry markets (LPMs) were analyzed. The three H10N8 cases had a history of poultry exposure and presented with high fever (>38°C), rapidly progressive pneumonia and lymphopenia. Substantial high levels of cytokines and chemokines were observed. The sequences from an isolate (A/Environment/Jiangxi/03489/2013 [H10N8]) in an epidemiologically linked LPM showed highly identity with human H10N8 virus, evidencing LPM as the source of human infection. The HA and NA of human and environmental H10N8 isolates showed high identity (99.1–99.9%) while six genotypes with internal genes derived from H9N2, H7N3 and H7N9 subtype viruses were detected in environmental H10N8 isolates. The genotype of the virus causing human infection, Jiangxi/346, possessed a whole internal gene set of the A/Environment/Jiangxi/10618/2014(H9N2)-like virus. Thus, our findings support the notion that LPMs can act as both a gene pool for the generation of novel reassortants and a source for human infection, and intensive surveillance and management should therefore be conducted.

Ustilaginoidea virens is a flower-infecting fungus that forms false smut balls in rice panicle. Rice false smut has long been considered a minor disease, but recently it occurred frequently and emerged as a major disease in rice production. In vitro co-cultivation of U. virens strain with young rice panicles showed that U. virens enters inside of spikelets from the apex and then grows downward to infect floral organs. In response to U. virens infection, rice host exhibits elevated ROS accumulation and enhanced callose deposition. The secreted compounds of U. virens can suppress rice pollen germination. Examination of sectioning slides of freshly collected smut balls demonstrated that both pistil and stamens of rice flower are infected by U. virens, hyphae degraded the contents of the pollen cells, and also invaded the filaments. In addition, U. virens entered rice ovary through the thin-walled papillary cells of the stigma, then decomposed the integuments and infected the ovary. The invaded pathogen could not penetrate the epidermis and other layers of the ovary. Transverse section of the pedicel just below the smut balls showed that there were no fungal hyphae observed in the vascular bundles of the pedicel, implicating that U. virens is not a systemic flower-infecting fungus.

The plant cell wall provides mechanical strength to support plant growth and development and to determine plant architecture. Cellulose and mixed-linkage glucan (MLG) present in primary cell wall, whereas cellulose, lignin and hemicellulose exist in secondary cell wall. Biosynthesis of the cell wall biopolymers needs the coordinated transcriptional regulation of all the biosynthetic genes. The module of OsmiR166b-OsHox32 regulates expression levels of the genes related to biosynthesis of MLG, cellulose and lignin. Transgenic plants knocking down miR166b (STTM166b) by short tandem target mimic (STTM) technology or overexpressing OsHox32 (OEHox32) showed drooping leaves and brittle culms. Due to accumulation of less lignin and cellulose, the cell wall thickness of STTM166b and OEHox32 plants was reduced when compared to that of wild-type plants. Overexpression of miR166b (OE166b) in rice plants or knocking down of OsHox32 by RNA interference (RNAiHox32) led to increased thickness of cell walls and enhanced mechanical strength of culms. Molecular analyses showed that OsmiR166b-OsHox32 pair regulates cell wall-related gene expression. OsHox32 binds to the promoters of OsCAD2 and OsCESA7 to suppress the expression levels of these two genes. The suppression of OsCAD2 is synergistic when OsHox32 is co-expressed with OSH15 (Oryza sativa homeobox 15). OsHox32 interacts with OSH15, and the START domain of OsHox32, harbouring the miR166b cleavage site, is required for the interaction of these two proteins. Our results demonstrate that OsmiR166b-OsHox32 pair plays important roles not only in plant growth and development but also in plant architecture by regulating the cell wall-related gene expression.