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Insights into the Sec-dependent effectors of Candidatus Liberibacter asiaticus and development of novel control strategy against citrus HLB N. WANG (1) (1) University of Florida, U.S.A.
Citrus Huanglongbing (HLB) is currently the most destructive disease on citrus worldwide. The causal agent for HLB in USA is Candidatus Liberibacter asiaticus (Las), a phloem-limited fastidious α-proteobacterium, which is transmitted by Asian citrus psyllids (ACP, Diaphorina citri). Interestingly, Las contains a complete General Secretory Pathway (GSP/Sec-translocon), which can be a potent system for the transportation of Las proteins including the virulence factors into the extracytoplasmic milieu. In this study we characterize the Sec-translocon dependent, signal peptide containing extracytoplasmic proteins of Las. A total of 150 proteins of Las_psy62 strain were predicted to contain signal peptides targeting them out of the cell cytoplasm via the Sec-translocon. For experimental validation of the predicted extracytoplasmic proteins, Escherichia coli based alkaline phosphatase (PhoA) gene fusion assays were conducted. A total of 89 out of the 150 predicted Las proteins were experimentally validated to contain signal peptides. We hypothesized that some of the Sec-dependent extracytoplasmic proteins are putative effectors. Those putative effectors were transgenically expressed in citrus to identify their putative targets for HLB development. To develop correspondent control strategy, we have adapted Cas9/sgRNA to modify the citrus genome to modify effector targets. We aim to generate HLB resistant or tolerant plants by disrupting the interaction between Sec-dependent effectors (SDEs) and their targets in citrus. In addition, we also developed antimicrobials to inhibit the SecA in the Sec pathway. SecA, an ATPase, is vital for the function of the Sec pathway and a good target to develop antimicrobials. We have identified multiple SecA inhibitors with high antibacterial activity to Liberibacters and their relatives.
Abstract Number:
S1-5 Session Type:
Special Session
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