Coevolution between the pathogen and host plant drives pathogenic effector diversity. However, the molecular mechanism behind host-specific pathogenesis remains to be explored. Here, we present a 43 Mb whole-genome sequence ofEndomelanconiopsis endophyticastrain LS29, a host-specific pathogen of the common subtropical treeCastanopsis fissa. We described its genome annotations and identified its effector candidates. By performing temporal transcriptome sequencing ofE. endophyticaonC. fissaduring early infection, we found thatE. endophyticarepressed other microbes in order to attack the tissue of the host by producing antibiotics earlier than 24 h post-inoculation (hpi). Simultaneously, a variety of effectors were secreted to recognize the host plant, but most of them showed a significantly opposing expression regulation trend after 24 hpi, indicating that 24 hpi represents a key time point between host recognition and specific infection. Furthermore, a comparison of isoenzymes showed that only a few effectors were identified as specific effectors, which were involved in hydrolyzing the compounds of the plant cell wall and releasing fatty acids during the early infection ofC. fissa. Our results determined host recognition timing and identified a specific catalog of effectors, which are crucial for revealing the molecular mechanism of host-specific pathogenesis.Keywords:comparative transcriptomics;effector;genomics;specific infection;whole-genome sequence
The distinctive bitter profile of Castanopsis fissa honey (LSZH) has not yet been clearly characterized at the chemical and molecular levels. Based on the LSZH samples ( n = 6), this study investigated bitterness-associated compounds and their potential receptor interactions by integrating sensory evaluation, machine learning, untargeted metabolomics, electronic tongue analysis, targeted UPLC-QQQ-MS/MS quantification, and molecular docking. A Random Forest model combined with untargeted metabolomics screened 71 candidate bitter compounds, among which alkaloid-related metabolites were prominently represented. Electronic tongue analysis showed that several compounds exhibited higher bitterness-related sensor responses than quinine under the tested conditions. Targeted UPLC-QQQ-MS/MS analysis identified and quantified five key compounds, among which kynurenic acid was the most abundant, reaching approximately 4500 ppm (mg/kg). Molecular docking suggested that these compounds could favorably interact with the human bitter taste receptor TAS2R46, with binding affinities ranging from −5.4 to −6.5 kcal/mol, mainly through hydrogen bonding, hydrophobic interactions, and π-related interactions. Overall, this study provides chemical evidence and mechanistic clues for understanding the bitterness of LSZH and offers an integrated analytical framework for screening bitterness-associated compounds in complex food systems.