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Anna Block

Researcher at United States Department of Agriculture

Publications -  52
Citations -  2690

Anna Block is an academic researcher from United States Department of Agriculture. The author has contributed to research in topics: Arabidopsis & Pseudomonas syringae. The author has an hindex of 23, co-authored 44 publications receiving 2188 citations. Previous affiliations of Anna Block include University of Nebraska–Lincoln & Agricultural Research Service.

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Characterization of three members of the Arabidopsis carotenoid cleavage dioxygenase family demonstrates the divergent roles of this multifunctional enzyme family

TL;DR: CCD1 distinguishes itself from other reported CCDs as being the only member not targeted to the plastid, and may have a role in synthesis of apocarotenoid flavor and aroma volatiles, especially in maturing seeds where loss of function leads to significantly higher carotenoids levels.
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Phytopathogen type III effector weaponry and their plant targets.

TL;DR: The wide array of strategies that bacterial pathogens employ to suppress innate immunity suggest that circumvention of innate immunity is crucial for bacterial pathogenicity of plants.
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The use of vapor phase extraction in metabolic profiling of phytohormones and other metabolites.

TL;DR: A novel metabolic profiling approach to the analysis of acidic phytohormones and other metabolites based on a simplistic preparation scheme and analysis by chemical ionization-gas chromatography/mass spectrometry is presented and directions for further method expansion are provided.
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Plant targets for Pseudomonas syringae type III effectors: Virulence targets or guarded decoys?

TL;DR: The phytopathogenic bacterium Pseudomonas syringae can suppress both pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggers immunity (ETI) by the injection of type III effector proteins into host cells.
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Multiple Hormones Act Sequentially to Mediate a Susceptible Tomato Pathogen Defense Response

TL;DR: Tomato actively regulates the Xcv-induced disease response via the sequential action of at least three hormones, promoting expansive cell death of its own tissue.