Publications by authors named "Boya Du"

Cyclic nucleotide-gated channel 5 (CNGC5), CNGC6, and CNGC9 (CNGC5/6/9 for simplicity) control Arabidopsis root hair (RH) growth by mediating the influx of external Ca to establish and maintain a sharp cytosolic Ca gradient at RH tips. However, the underlying mechanisms for the regulation of CNGCs remain unknown. We report here that calcium dependent protein kinase 1 (CPK1) directly activates CNGC5/6/9 to promote Arabidopsis RH growth.

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is an important protozoan parasite that causes abortion in cattle and nervous system dysfunction in dogs. No effective drugs and vaccines for neosporosis are available. Further elucidation of proteins related to virulence will provide potential candidates for vaccine development against neosporosis.

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Jasmonates (JAs) are a class of oxylipin phytohormones including jasmonic acid (JA) and derivatives that regulate plant growth, development and biotic and abiotic stress. A number of transporters have been identified to be responsible for the cellular and subcellular translocation of JAs. However, the mechanistic understanding of how these transporters specifically recognize and transport JAs is scarce.

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Multiple cyclic nucleotide-gated channels (CNGCs) are abscisic acid (ABA)-activated Ca2+ channels in Arabidopsis (Arabidopsis thaliana) guard cells. In particular, CNGC5, CNGC6, CNGC9, and CNGC12 are essential for ABA-specific cytosolic Ca2+ signaling and stomatal movements. However, the mechanisms underlying ABA-mediated regulation of CNGCs and Ca2+ signaling are still unknown.

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Neospora caninum, an obligate intracellular parasitic protozoan discovered by Dubey in 1988, is the pathogen of neosporosis, which causes neurological symptoms in dogs and abortions in cows. Since there is no effective drug or vaccine against N. caninum, a deeper understanding of the molecules critical to parasite survival inside host cells is necessary.

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Toxoplasma gondii is an obligate intracellular protozoan that causes toxoplasmosis. Previous studies have shown that the perturbation of mitochondrial metabolism in T. gondii results in growth deficiency in host cells and lack of virulence in animals.

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