The
biocontrol activity and chemical composition of the volatile
organic compounds (VOCs) produced by Pseudomonas chlororaphis subsp. aureofaciens SPS-41 were investigated. The
VOCs inhibited mycelial growth and spore germination in Ceratocystis
fimbriata, which causes black rot disease in sweet potato
tuber roots (TRs) and showed wide-spectrum antifungal activity against
several plant pathogenic fungi. A microscopic examination of C. fimbriata cells suggested morphological changes and a
loss of cellular contents. Different inoculation strategies significantly
affected the antifungal activity of the VOCs. In the volatile profile
of SPS-41, the most abundant compound, 3-methyl-1-butanol, followed
by phenylethyl alcohol and 2-methyl-1-butanol showed strong inhibition
toward C. fimbriata. The weight loss rate and disease
severity of the TRs were significantly reduced in response to the
VOCs emitted by SPS-41. The results suggest that the VOCs produced
by P. chlororaphis subsp. aureofaciens SPS-41 might constitute an attractive biological fumigant for controlling
black rot disease in sweet potato TRs.
In mammalian cells, autophagy plays crucial roles in restricting further spread of invading bacterial pathogens. Previous studies have established that the virulence factors SseF and SseG are required for intracellular bacterial survival and replication. However, the underlying mechanism by which these two effectors facilitate bacterial infection remains elusive. Here, we report that SseF and SseG secreted by Typhimurium ( Typhimurium) inhibit autophagy in host cells and thereby establish a replicative niche for the bacteria in the cytosol. Mechanistically, SseF and SseG impaired autophagy initiation by directly interacting with the small GTPase Rab1A in the host cell. This interaction abolished Rab1A activation by disrupting the interaction with its guanine nucleotide exchange factor (GEF), the TRAPPIII (transport protein particle III) complex. This disruption of Rab1A signaling blocked the recruitment and activation of Unc-51-like autophagy-activating kinase 1 (ULK1) and decreased phosphatidylinositol 3-phosphate biogenesis, which ultimately impeded autophagosome formation. Furthermore, SseF- or SseG-deficient bacterial strains exhibited reduced survival and growth in both mammalian cell lines and mouse infection models, and Rab1A depletion could rescue these defects. These results reveal that virulence factor-dependent inactivation of the small GTPase Rab1A represents a previously unrecognized strategy of Typhimurium to evade autophagy and the host defense system.
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