MyD88 knockdown by RNAi prevents bacterial stimulation of tubeworm metamorphosis

• 成果类型: Article
• 署名作者: Darin, Emily; Farrell, Morgan v; Ali, Tatyana N.; Alfaro, Josefa Rivera; Malter, Kyle E.; Shikuma, Nicholas J.
• 署名单位: California State University System; San Diego State University; California State University System; San Diego State University
• 刊物名称: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
• ISSN/ISSBN: 0027-13566
• DOI: 10.1073/pnas.2505805122
• 发表日期: 2025-06-10
• 关键词: pseudomonas-aeruginosa pa14; hydroids-elegans; expression; immunity; genes; interference; inflammation; mechanisms; ingestion; produce

摘要

Diverse animals across the tree of life undergo the life- history transition of metamorphosis in response to bacteria. Although immunity has been implicated in this metamorphosis in response to bacteria, no functional connection has yet been demonstrated between immunity and metamorphosis. We investigated a host-microbe interaction involving Pseudoalteromonas luteoviolacea, a metamorphosis- inducing marine bacterium. By creating a marine bacteria-mediated RNA interference approach, we show that myeloid differentiation factor 88 (MyD88), a critical immune adaptor for Toll- like receptor and interleukin pathways, is necessary for the stimulation of metamorphosis in response to bacteria. In addition to a developmental role, we show that MyD88 is necessary for survival during exposure during both development and an immune response. These results provide a functional characterization of the innate immune system involved in an animal's metamorphosis.