Carbohydrate translocation determines the phenolic content of Populus foliage: a test of the sink-source model of plant defense.

• Here, we examine the influence of source-to-sink carbohydrate (CHO) flow on the development of constitutive and inducible levels of phenylpropenoids in hybrid poplar (Populus nigra × P. deltoides) foliage to determine if secondary metabolic processes in plant modules can be inhibited in a predictable manner by events such as herbivory and the development of new leaves and reproductive structures, which alter the path of phloem-borne resources. • Phenylpropenoid concentrations were determined for developing foliage after CHO flow, measured as the translocation of 13 C from labeled sources was manipulated. • Phenylpropenoid metabolism in both unwounded and induced sink leaves was directly and positively linked to rates of CHO import. Alterations in rates of translocation yielded different results, depending on how CHO import was affected: the removal of competing sinks rapidly and dramatically increased leaf phenolic contents, whereas phenolic levels (and their inducibility) tended to be reduced when import was interrupted. • High and inducible sink strength in developing poplar leaves provides resources for phenolic biosynthesis and, as a result, restrictions or re-directions of CHOs affect the foliar quality. Sink strength and the vascular architecture of plants, which confer upon them a modular nature, can determine the direction and magnitude of defense responses in trees.

Th17 cells and IL-17 receptor signaling are essential for mucosal host defense against oral candidiasis.

The commensal fungus Candida albicans causes oropharyngeal candidiasis (OPC; thrush) in settings of immunodeficiency. Although disseminated, vaginal, and oral candidiasis are all caused by C. albicans species, host defense against C. albicans varies by anatomical location. T helper 1 (Th1) cells have long been implicated in defense against candidiasis, whereas the role of Th17 cells remains controversial. IL-17 mediates inflammatory pathology in a gastric model of mucosal candidiasis, but is host protective in disseminated disease. Here, we directly compared Th1 and Th17 function in a model of OPC. Th17-deficient (IL-23p19(-/-)) and IL-17R-deficient (IL-17RA(-/-)) mice experienced severe OPC, whereas Th1-deficient (IL-12p35(-/-)) mice showed low fungal burdens and no overt disease. Neutrophil recruitment was impaired in IL-23p19(-/-) and IL-17RA(-/-), but not IL-12(-/-), mice, and TCR-alphabeta cells were more important than TCR-gammadelta cells. Surprisingly, mice deficient in the Th17 cytokine IL-22 were only mildly susceptible to OPC, indicating that IL-17 rather than IL-22 is vital in defense against oral candidiasis. Gene profiling of oral mucosal tissue showed strong induction of Th17 signature genes, including CXC chemokines and beta defensin-3. Saliva from Th17-deficient, but not Th1-deficient, mice exhibited reduced candidacidal activity. Thus, the Th17 lineage, acting largely through IL-17, confers the dominant response to oral candidiasis through neutrophils and antimicrobial factors.

Protein interactions among the vaccinia virus late transcription factors.

The viral proteins A1L, A2L, G8R, and H5R positively modulate vaccinia virus late gene expression. Host-encoded proteins hnRNP A2 and RBM3 may also interact with these viral factors to influence late gene expression. In these studies, a yeast two-hybrid screen and in vitro pulldown and crosslinking experiments were used to investigate protein--protein interactions among these factors. These studies confirmed a previous observation that G8R interacts with itself and A1L. However, self-interactions of A1L and H5R, and interactions between A2L and G8R, A2L and H5R, and H5R and G8R were also observed. In addition, the proteins hnRNP A2 and RBM3 both showed some interaction with A2L. Illustration of these interactions is a step toward understanding the architecture of the late gene transcription complex as it occurs in poxviruses.