Expression of hrp (hypersensitive reaction and pathogenicity) genes inside the host is crucial for virulence of phytopathogenic bacteria. The hrp genes encode components of type3 secretion system (T3SS), HR elicitors and several regulators, which are involved in the co-ordinated expression of hrp genes in the host environment and in hrp inducing chemically defined medium. However, little is known about specific host or environmental factors which may play a role in the induction of hrp gene expression. In this study, we show that iron-limiting condition elicits induced expression of hrp genes, including type3 secretion system (T3SS) and effectors (T3E). Expression analysis using qRT-PCR and promoter probe strains suggest significant induction in the expression of Hrp and T3S-associated genes of Xanthomonas campestris pv. campestris (Xcc) under low-iron condition, and is suppressed by exogenous supplementation of iron. Furthermore, we show that with exogenous iron supplementation, wild type Xcc exhibited reduced disease symptoms in host-plant, and exhibited significant reduction in HR and callose deposition in the non-host plants. Xanthomonas oryzae and oryzicola pathovars also exhibited the iron affect, albeit to a lesser extend compared with the Xcc. Overall, our results suggest that low-iron condition inside the host may play a crucial role in pathogenicity.
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http://dx.doi.org/10.1111/1758-2229.12650 | DOI Listing |
PLoS Genet
January 2025
Department of Biology, Boston University, Boston Massachusetts, United States of America.
The death and clearance of nurse cells is a consequential milestone in Drosophila melanogaster oogenesis. In preparation for oviposition, the germline-derived nurse cells bequeath to the developing oocyte all their cytoplasmic contents and undergo programmed cell death. The death of the nurse cells is controlled non-autonomously and is precipitated by epithelial follicle cells of somatic origin acquiring a squamous morphology and acidifying the nurse cells externally.
View Article and Find Full Text PDFMalar J
December 2024
Centro de Investigação em Saúde de Manhiça, Maputo, Mozambique.
Background: Rapid diagnostic tests (RDTs) based on the detection of Plasmodium falciparum histidine rich protein 2 (PfHRP2) are widely used for the diagnostic of P. falciparum in Africa. However, deletions of the pfhrp2 and pfhrp3 genes can lead to false negative test results and compromise appropriate case management.
View Article and Find Full Text PDFRapid diagnostic tests (RDTs) are crucial for diagnosing malaria in resource-limited settings. These tests, which detect the histidine-rich protein 2 (PfHRP2) and its structural homologue PfHRP3, are specifically designed to identify Plasmodium falciparum. Deletion of the Pfhrp2 gene in parasite has been reported in India and other malaria-endemic countries.
View Article and Find Full Text PDFBMJ Open
November 2024
Centro de Investigação em Saúde de Manhiça (CISM), Manhiça, Mozambique
Introduction: Malaria molecular surveillance has the potential to generate information on biological threats that compromise the effectiveness of antimalarial interventions. This study aims to streamline surveillance activities to inform the new strategic plan of the Mozambican National Malaria Control Programme (2023-2030) for malaria control and elimination.
Methods And Analyses: This prospective genomic surveillance study aims to generate genetic data to monitor diagnostic failures due to deletions and molecular markers of antimalarial drug resistance, to characterise transmission sources and to inform the implementation of new antimalarial approaches to be introduced in Mozambique (chemoprevention and child malaria vaccination).
Sheng Wu Gong Cheng Xue Bao
October 2024
College of Life Sciences, Zhejiang Normal University, Jinhua 321004, Zhejiang, China.
The zinc uptake regulator (Zur) has highly conserved sequences in the plant pathogen , while its functions are diverse in different strains or races. To elucidate the functions of Zur in pv. (), we constructed a -deleted mutant (Δ) by homologous recombination.
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