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X-WR-CALNAME;VALUE=TEXT:HUH Seminar Series - Wayne M. Jurick II
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SUMMARY:HUH Seminar Series - Wayne M. Jurick II
DESCRIPTION:<p>	<strong>Dr. Wayne M Jurick II<br><span><span style="line-height:107%"><span>Lead Scientist and </span></span></span></strong><strong>Research Plant Pathologist<br>USDA Agricultural Research Service, Food Quality Laboratory</strong></p><p>	<strong>Title</strong>: An intriguing tale of a non-host specific mycotoxin: Plant cell death, ecological impacts, active efflux and leveraging culture collections for plant-fungal-microbe-interactions<!--break--></p><p>	<strong>Abstract</strong>: Non-host specific mycotoxins (e.g. patulin, cercosporin, tentoxin) are produced by fungi. They are toxic small molecules that aid host-pathogen interactions and are produced by saprophytes, phytopathogens, and opportunistic human pathogens. However, their function in the broader biological context regarding their impact on the host, mechanism of self-tolerance, and ecological role(s) are largely unexplored. To answer these questions, the polyketide lactone patulin, produced by<em> Penicillium</em> spp. during postharvest pome fruit decay, serves as a genetically tractable, economically important system. Our findings shows that patulin functions as a non-specific toxin that mimics some symptoms of decay in a dose-dependent, cultivar independent manner. The toxin interferes with early conidial germination and germ tube elongation in 6 different <em>Penicillium </em>spp. isolates with varying levels of sensitivity. However, all formed normal colonies after 7 days. In contrast, 4 fungal phytopathogens were inhibited and did not form colonies after 7 days. Thus, indicating the toxin may serve to exclude other pathogens occurring on the apple surface and stop them from joining the infection court buffet. Mechanism of auto-tolerance in <em>Penicillium </em>spp. was exploited using a broad-spectrum efflux pump inhibitor which resulted in increased sensitivity to patulin application. Future studies will focus on the mechanistic basis of auto-resistance in <em>Penicillium </em>spp. and elucidate genetic factors in susceptible fungal phytopathogens/model plants. Additionally, we aim to leverage unexplored microbial collections to screen for molecular switches, novel enzymes to degrade patulin, and identify new antagonists as biological control agents to control blue mold. Our findings provide as solid foundation of formative work to explore patulin mode-of-action studies with the long-term goal of developing novel toxin and blue mold decay mitigation strategies.</p><p>	<strong>Join via Zoom livestream: <a href="https://harvard.zoom.us/j/96367794053?pwd=VlRsOHp4bCs1OFR5dHVRRU93TG1RZz09">https://bit.ly/3IFHI2B</a></strong></p><p>	 </p>
LOCATION:22 Divinity Avenue, Cambridge, MA 02138, HUH Seminar Room 125 or live-stream
STATUS:CONFIRMED
DTSTART:20230321T160000Z
DTEND:20230321T170000Z
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