Genome-Wide Profiling and Phylogenetic Analysis of the SWEET Sugar Transporter Gene Family in Walnut and Their Lack of Responsiveness to Xanthomonas arboricola pv. juglandis Infection.

Following photosynthesis, sucrose is translocated to sink organs, where it provides the primary source of carbon and energy to sustain plant growth and development. Sugar transporters from the SWEET (sugar will eventually be exported transporter) family are rate-limiting factors that mediate sucrose transport across concentration gradients, sustain yields, and participate in reproductive development, plant senescence, stress responses, as well as support plant-pathogen interaction, the focus of this study. We identified 25 SWEET genes in the walnut genome and distinguished each by its individual gene structure and pattern of expression in different walnut tissues. Their chromosomal locations, cis-acting motifs within their 5' regulatory elements, and phylogenetic relationship patterns provided the first comprehensive analysis of the SWEET gene family of sugar transporters in walnut. This family is divided into four clades, the analysis of which suggests duplication and expansion of the SWEET gene family in Juglans regia. In addition, tissue-specific gene expression signatures suggest diverse possible functions for JrSWEET genes. Although these are commonly used by pathogens to harness sugar products from their plant hosts, little was known about their role during Xanthomonas arboricola pv. juglandis (Xaj) infection. We monitored the expression profiles of the JrSWEET genes in different tissues of "Chandler" walnuts when challenged with pathogen Xaj417 and concluded that SWEET-mediated sugar translocation from the host is not a trigger for walnut blight disease development. This may be directly related to the absence of type III secretion system-dependent transcription activator-like effectors (TALEs) in Xaj417, which suggests different strategies are employed by this pathogen to promote susceptibility to this major aboveground disease of walnuts.

Comparison of standardized uptake value-based positron emission tomography and computed tomography target volumes in esophageal cancer patients undergoing radiotherapy.

PURPOSE: To study various standardized uptake value (SUV)-based approaches to ascertain the best strategy for delineating metabolic tumor volumes (MTV). METHODS AND MATERIALS: Twenty-two consecutive previously treated esophageal cancer patients with positron emission tomography (PET) imaging and computed tomography (CT)-based radiotherapy plans were studied. At the level of the tumor epicenter, MTVs were delineated at 11 different thresholds: SUV ≥2, ≥2.5, ≥3, ≥3.5 (SUV(n)); ≥40%, ≥45%, and ≥50% of the maximum (SUV(n%)); and mean liver SUV + 1, 2, 3, and 4 standard deviations (SUV(Lnσ)). The volume ratio and conformality index were determined between MTVs, and the corresponding CT/endoscopic ultrasound-based gross tumor volume (GTV) at the epicenter. Means were analyzed by one-way analysis of variance for repeated measures and further compared using a paired t test for repeated measures. RESULTS: The mean conformality indices ranged from 0.33 to 0.48, being significantly (p < 0.05) closest to 1 at SUV(2.5) (0.47 ± 0.03) and SUV(L4σ) (0.48 ± 0.03). The mean volume ratios ranged from 0.39 to 2.82, being significantly closest to 1 at SUV(2.5) (1.18 ± 0.36) and SUV(L4σ) (1.09 ± 0.15). The mean value of the SUVs calculated using the SUV(L4σ) approach was 2.4. CONCLUSIONS: Regardless of the SUV thresholding method used (i.e., absolute or relative to liver mean), a threshold of approximately 2.5 yields the highest conformality index and best approximates the CT-based GTV at the epicenter. These findings may ultimately aid radiation oncologists in the delineation of the entire GTV in esophageal cancer patients.

Non-human primate model of Kaposi's sarcoma-associated herpesvirus infection.

Since Kaposi's sarcoma-associated herpesvirus (KSHV or human herpesvirus 8) was first identified in Kaposi's sarcoma (KS) lesions of HIV-infected individuals with AIDS, the basic biological understanding of KSHV has progressed remarkably. However, the absence of a proper animal model for KSHV continues to impede direct in vivo studies of viral replication, persistence, and pathogenesis. In response to this need for an animal model of KSHV infection, we have explored whether common marmosets can be experimentally infected with human KSHV. Here, we report the successful zoonotic transmission of KSHV into common marmosets (Callithrix jacchus, Cj), a New World primate. Marmosets infected with recombinant KSHV rapidly seroconverted and maintained a vigorous anti-KSHV antibody response. KSHV DNA and latent nuclear antigen (LANA) were readily detected in the peripheral blood mononuclear cells (PBMCs) and various tissues of infected marmosets. Remarkably, one orally infected marmoset developed a KS-like skin lesion with the characteristic infiltration of leukocytes by spindle cells positive for KSHV DNA and proteins. These results demonstrate that human KSHV infects common marmosets, establishes an efficient persistent infection, and occasionally leads to a KS-like skin lesion. This is the first animal model to significantly elaborate the important aspects of KSHV infection in humans and will aid in the future design of vaccines against KSHV and anti-viral therapies targeting KSHV coinfected tumor cells.