Date of Graduation

12-2019

Document Type

Thesis

Degree Name

Master of Science in Plant Pathology (MS)

Degree Level

Graduate

Department

Entomology and Plant Pathology

Advisor/Mentor

Rojas, Clemencia M.

Committee Member

Lewis, Jeffrey A.

Second Committee Member

Egan, Martin J.

Keywords

Arabidopsisi thaliana; Bacterial effectors; HopD1; HopG1; Nonhost disease resistance; Pseudomonas syringae

Abstract

The pathogenicity of Pseudomonas syringae is associated with the type III secretion system (T3SS), a complex of proteins assembled in the inner and outer bacterial membranes that traverses the plant cell wall to deliver bacterial proteins into the cytoplasm of plant cells. The effector proteins translocated into the plant cells are called Hops (Hypersensitive response and pathogenicity outer proteins). Bacterial effectors target plant immune proteins to suppress defense responses and enhance bacterial parasitism. The Arabidopsis thaliana nonhost resistance 2B (AtNHR2B), a recently identified immune protein, is degraded after inoculation with the adapted pathogen of Arabidopsis, P. syringae pv tomato DC3000 (Pst DC3000), but not by the non-adapted pathogen P. syringae pv. tabaci (Pstab). Several Pst DC3000 effectors, including HopG1 and HopD1 interact with AtNHR2B in planta. Characterization of the effectors presence in plants upon inoculation with Pstab showed that transgenic expression of HopG1-FLAG triggered cell death, high electrolyte leakage levels and increased production of mitochondrial ROS. In contrast, HopG1-FLAG expression in combination with AtNHR2B-GFP caused susceptibility to Pstab as shown by the development of disease symptoms and the significant increase in bacterial growth. Together, these results suggest that HopG1 targets AtNHR2B to interfere with plant immune response upon bacterial infection. In contrast, transgenic plants expressing HopD1-HA alone or in combination with AtNHR2B-GFP, showed disease symptoms after inoculation with Pstab, that normally does not cause disease in wild-type Col-0 plants. Moreover, Pstab grew significantly more in transgenic plants overexpressing HopD1-HA than in wild-type Col-0. Interestingly, Arabidopsis plants expressing the bacterial effector HopD1-HA alone or in combination with AtNHR2B-GFP were deficient in callose deposition and showed a downregulation of the callose synthase gene PMR4. Altogether, these results suggest that HopD1 interferes with callose deposition and by doing so hinders defense responses.

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