Host range of the ginger strain of Pseudomonas solanacearum in Queensland

The host range of Pseudomonas solanacearum biotype 4, the strain responsible for a rapid wilt of ginger, was found to include tomato, potato, capsicum, egg plant, peanut, tobacco, Solanum nigrum, Physalis minima, P. peruviana, and Solanm mauritianum. During the summer months of 1967-68 and 1969-70, weeds growing in bacterial wilt affected ginger plantings were examined for the presence of P. solanacearum. Biotype 4 was isolated from S. nigrum, Crassocephalum crepidioides, S. mauritianum, P. minima, P. peruviana, and Ageratum houstonianum. Biotype 3, the strain commonly found in the ginger growing district of southern Queensland was isolated from S. nigrum, C. crepidioides, S. mauritianum, Xanthium pungens, Dodonaea lanceolata, Bidens pilosa, and Sida spinosa. These weeds were all collected from ginger fields. It appears from these results and previous observations that biotype 4 has a more restricted and slightly different host range from biotype 3. Consequently it has been suggested that in any crop rotation, ginger growers should eliminate known biotype 4 susceptible weeds. Both biotypes 4 and 3 survived, in the experimental plots, a 20-month period of severe drought during 1968-69. However, no attempt was made to control weed growth in the trial area

A new bacterial leaf spot of antirrhinum seedlings caused by a subspecies of Pseudomonas fluorescent Migula, 1895

Morphological, cultural and biochemical characteristics of an organism designated P. fluorescens var. antirrhinastri, which has caused serious losses among antirrhinum seedlings raised in Queensland

Resistance to common bacterial blight in selected accessions of Phaseolus species

Nine P. accessions showed consistent reactions to common bacterial blight (Xanthomonas campestris pv. phaseoli) in 2 field trials and 1 greenhouse test

Cd4+ T cell-specific proteomic pathways identified in progression of hypertension across postmenopausal transition

BACKGROUND: Menopause is associated with an increase in the prevalence and severity of hypertension in women. Although premenopausal females are protected against T cell-dependent immune activation and development of angiotensin II (Ang II) hypertension, this protection is lost in postmenopausal females. Therefore, the current study hypothesized that specific CD4+ T cell pathways are regulated by sex hormones and Ang II to mediate progression from premenopausal protection to postmenopausal hypertension. METHODS AND RESULTS: Menopause was induced in C57BL/6 mice via repeated 4-vinylcyclohexene diepoxide injections, while premenopausal females received sesame oil vehicle. A subset of premenopausal mice and all menopausal mice were infused with Ang II for 14 days (Control, Ang II, Meno/Ang II). Proteomic and phosphoproteomic profiles of CD4+ T cells isolated from spleens were examined. Ang II markedly increased CD4+ T cell protein abundance and phosphorylation associated with DNA and histone methylation in both premenopausal and postmenopausal females. Compared with premenopausal T cells, Ang II infusion in menopausal mice increased T cell phosphorylation of MP2K2, an upstream regulator of ERK, and was associated with upregulated phosphorylation at ERK targeted sites. Additionally, Ang II infusion in menopausal mice decreased T cell phosphorylation of TLN1, a key regulator of IL-2Rα and FOXP3 expression. CONCLUSIONS: These findings identify novel, distinct T cell pathways that influence T cell-mediated inflammation during postmenopausal hypertension. © 2021 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]