Bee Research Laboratory, Agricultural Research Service of the United States Department of Agriculture, Beltsville, Maryland, United States of America.
PLoS One. 2013 Jun 6;8(6):e65424. doi: 10.1371/journal.pone.0065424. Print 2013.
American foulbrood disease of honey bees is caused by the bacterium Paenibacillus larvae. Infection occurs per os in larvae and systemic infection requires a breaching of the host peritrophic matrix and midgut epithelium. Genetic variation exists for both bacterial virulence and host resistance, and a general immunity is achieved by larvae as they age, the basis of which has not been identified. To quickly identify a pool of candidate genes responsive to P. larvae infection, we sequenced transcripts from larvae inoculated with P. larvae at 12 hours post-emergence and incubated for 72 hours, and compared expression levels to a control cohort. We identified 75 genes with significantly higher expression and six genes with significantly lower expression. In addition to several antimicrobial peptides, two genes encoding peritrophic-matrix domains were also up-regulated. Extracellular matrix proteins, proteases/protease inhibitors, and members of the Osiris gene family were prevalent among differentially regulated genes. However, analysis of Drosophila homologs of differentially expressed genes revealed spatial and temporal patterns consistent with developmental asynchrony as a likely confounder of our results. We therefore used qPCR to measure the consistency of gene expression changes for a subset of differentially expressed genes. A replicate experiment sampled at both 48 and 72 hours post infection allowed further discrimination of genes likely to be involved in host response. The consistently responsive genes in our test set included a hymenopteran-specific protein tyrosine kinase, a hymenopteran specific serine endopeptidase, a cytochrome P450 (CYP9Q1), and a homolog of trynity, a zona pellucida domain protein. Of the known honey bee antimicrobial peptides, apidaecin was responsive at both time-points studied whereas hymenoptaecin was more consistent in its level of change between biological replicates and had the greatest increase in expression by RNA-seq analysis.
美洲幼虫腐臭病是由幼虫芽孢杆菌引起的。幼虫经口感染,系统感染需要突破宿主的围食膜和中肠上皮。细菌毒力和宿主抗性都存在遗传变异,幼虫随着年龄的增长会产生一般免疫力,但其基础尚未确定。为了快速鉴定出一组对幼虫芽孢杆菌感染有反应的候选基因,我们对孵化后 12 小时接种幼虫芽孢杆菌并培养 72 小时的幼虫进行了转录组测序,并将表达水平与对照组进行了比较。我们发现 75 个基因的表达显著上调,6 个基因的表达显著下调。除了几种抗菌肽外,两种编码围食膜结构域的基因也被上调。细胞外基质蛋白、蛋白酶/蛋白酶抑制剂和 Osiris 基因家族成员在差异表达基因中较为常见。然而,对差异表达基因的果蝇同源物进行分析表明,空间和时间模式与发育不同步一致,这可能是我们结果的混杂因素。因此,我们使用 qPCR 来测量一组差异表达基因的表达变化的一致性。在感染后 48 小时和 72 小时采样的重复实验进一步区分了可能参与宿主反应的基因。我们的测试集中一致响应的基因包括膜翅目特异性蛋白酪氨酸激酶、膜翅目特异性丝氨酸内肽酶、细胞色素 P450(CYP9Q1)和 trynity 的同源物,trynity 是一种透明带结构域蛋白。在已知的蜜蜂抗菌肽中, hymenoptaecin 在研究的两个时间点都有反应,而 hymenoptaecin 在其生物学重复之间的变化水平更一致,并且在 RNA-seq 分析中表达水平的增加最大。