摘要

苏云金芽孢杆菌促进了许多经济上重要的作物的生长。本研究提出了苏云金芽孢杆菌ATCC 10792型菌株中存在的巨型质粒的完整基因组序列，这是一种典型的具有杀虫活性的孢子形成革兰氏阳性菌，并研究其遗传特征。使用Pac-Bio测序仪和分层基因组装配过程分别对基因组进行测序和组装。进行了进一步的基因组注释，鉴定了总共489种蛋白质和具有584,623bp的新型大质粒（poh1）。 poh1的组织揭示了参与杀虫毒素途径的基因。负责抗微生物，杀虫和抗生素活性的基因在poh1中非常保守，表明与植物宿主密切相关。 poh1质粒含有编码新型晶体蛋白激酶的基因，该激酶负责产生zeta毒素，zeta毒素通过肽聚糖合成的全面抑制使毒物和其他革兰氏阴性细菌中毒。 Lantibiotics是一组细菌素，包括生物活性抗菌肽Paenibacillin。此外，poh1还含有编码短杆菌肽S原型抗生素肽和四环素抗性蛋白的基因。总之，苏云金芽孢杆菌菌株ATCC 10792的菌株特异性基因通过基于主要致病因子的完整基因组测序和生物信息学数据进行鉴定，这些数据有助于进一步研究致病机制和表型分析。

Bacillus thuringiensis promotes the growth of numerous economically important crops. The present study presents the complete genome sequence for a mega plasmid present in the type strain of B. thuringiensis ATCC 10792, a typical spore-forming Gram-positive bacterium with insecticidal activity, and investigates its genetic characteristics. The genome was sequenced and assembled de novo using Pac-Bio sequencers and the Hierarchical Genome Assembly Process, respectively. Further genome annotation was performed, and a total of 489 proteins and a novel mega-plasmid (poh1) with 584,623 bps were identified. The organization of poh1 revealed the genes involved in the insecticidal toxin pathway. The genes responsible for antimicrobial, insecticidal and antibiotic activities were well conserved in poh1, indicating an intimate association with plant hosts. The poh1 plasmid contains the gene encoding a novel crystal protein kinase responsible for production of zeta toxin, which poisons insects and other Gram-negative bacteria through the global inhibition of peptidoglycan synthesis. Lantibiotics are a group of bacteriocins that include the biologically active antimicrobial peptide Paenibacillin. Further, poh1 also contains the genes that encode the gramicidin S prototypical antibiotic peptide and tetracycline resistance protein. In conclusion, the strain-specific genes of B. thuringiensis strain ATCC 10792 were identified through complete genome sequencing and bioinformatics data based on major pathogenic factors that contribute to further studies of the pathogenic mechanism and phenotype analyses.

https://www.ncbi.nlm.nih.gov/pubmed/30326263