Cucurbit downy mildew (CDM) is a destructive disease in cucurbits in the United States (U.S.) caused by Pseudoperonospora cubensis. Pseudoperonospora cubensis (Berk. & M.A. Curtis) Rostovez is the leading obligate biotroph with the highest risk of developing resistance to fungicides. Downy mildew (DM) pathogens cause significant crop losses worldwide to many cropping systems. Disease management of CDM has become increasingly complicated as repeated application of fungicides in the growing season increases the selection pressure favorably towards the development of resistant mutants and reduced fungicide efficacy due to the aggressiveness of the pathogen has increased the yield losses. Control of P. cubensis is very difficult due its ability to overcome control measures quickly for example, host resistance, fungicides and long dispersal capabilities. It is very important to monitor this pathogen populations continuously to determine the sensitivity of fungicide. Host-adapted clades have been described in P. cubensis with clade 1 mainly infecting squash (Cucurbita pepo), Citrullus lanatus (watermelon), and Cucurbita maxima (pumpkin), and clade 2 mainly infecting Cucumis sativus (cucumber), and Cucumis melo (cantaloupe). The host-adapted clades have been also linked to differences in the occurrence of fungicide resistance mutations related to carboxylic acid amides (CAA) but not quinone outside inhibitors (QoI).
The quinone outside inhibitor (QoI), strobilurin fungicides (FRAC 11) bind to the cytochrome bc1 enzyme complex III, which restrict mitochondrial respiration through inhibiting electron transfer, resulted in termination of cellular respiration, and production of ATP. The G143A substitution in the cytochrome b (cytb) gene confer resistance in P. cubnesis which is due to a single nucleotide polymorphism (SNP) responsible for an amino acid substitution from glycine to alanine at position 143. Carboxylic acid amide (CAA) fungicides (FRAC 40) are widely used in controlling downy mildew, regulates cellulase biosynthesis in oomycetes, which targets the cellulose synthase 3 (CesA3). Single site fungicides (a.i., oxathiapiprolin) have medium to high risk of fungicide resistance, which targets the oxysterol binding protein in oomycetes and effective in all life stages of P. cubensis. Systemic fungicides (single site) have higher risk of resistance development as they are active in one point of metabolic pathway of the pathogen. Multisite inhibitors (contract fungicides) have lower risk of development of fungicides against P. cubensis populations. Fungicide sensitivity can quickly change in P. cubensis populations, for example, fluopicolide and propamocarb in some years.
Currently at NC State University I’m doing research into genomics of downy mildew disease of cucurbits caused by Pseudoperosnospora cubensis, focusing on the detection of fungicides resistance mutation, host-adapted clade assays of the Pseudoperosnospora cubensis, the phylogeny and evolution of the Pseudoperosnospora cubensis populations, and the effects of population dynamics on disease epidemiology in different cucurbitaceous hosts to improve the current CDM management program in the U.S.
In my PhD study at North Dakota State University, I performed extensive research into basic and applied biology and the infection mechanisms of pathogens, molecular host-pathogen interactions, and the characterization of pathogens and integrated disease management of sugar beet diseases. I received my BSc in agriculture and an MS in plant pathology from Sher-e-Bangla Agricultural University in Bangladesh and served as a faculty in the same university in Plant Pathology department for more than 6 years. During my service, I was involved in research, teaching and extension for vegetable, cereals and fruit crop diseases.
PhD, Plant Pathology, North Dakota State University (2022)
MS, Plant Pathology, Shere-e-Bangla Agricultural University, Bangladesh (2012)
B Sc Ag (Hons.), Shere-e-Bangla Agricultural University, Bangladesh (2009)