Wright Rachel M, Aglyamova Galina V, Meyer Eli, Matz Mikhail V
Institute for Cell and Molecular Biology, The University of Texas at Austin, Austin, USA.
Department of Integrative Biology, The University of Texas at Austin, Austin, USA.
BMC Genomics. 2015 May 9;16(1):371. doi: 10.1186/s12864-015-1540-2.
Corals are capable of launching diverse immune defenses at the site of direct contact with pathogens, but the molecular mechanisms of this activity and the colony-wide effects of such stressors remain poorly understood. Here we compared gene expression profiles in eight healthy Acropora hyacinthus colonies against eight colonies exhibiting tissue loss commonly associated with white syndromes, all collected from a natural reef environment near Palau. Two types of tissues were sampled from diseased corals: visibly affected and apparently healthy.
Tag-based RNA-Seq followed by weighted gene co-expression network analysis identified groups of co-regulated differentially expressed genes between all health states (disease lesion, apparently healthy tissues of diseased colonies, and fully healthy). Differences between healthy and diseased tissues indicate activation of several innate immunity and tissue repair pathways accompanied by reduced calcification and the switch towards metabolic reliance on stored lipids. Unaffected parts of diseased colonies, although displaying a trend towards these changes, were not significantly different from fully healthy samples. Still, network analysis identified a group of genes, suggestive of altered immunity state, that were specifically up-regulated in unaffected parts of diseased colonies.
Similarity of fully healthy samples to apparently healthy parts of diseased colonies indicates that systemic effects of white syndromes on A. hyacinthus are weak, which implies that the coral colony is largely able to sustain its physiological performance despite disease. The genes specifically up-regulated in unaffected parts of diseased colonies, instead of being the consequence of disease, might be related to the originally higher susceptibility of these colonies to naturally occurring white syndromes.
珊瑚能够在与病原体直接接触的部位启动多种免疫防御,但这种活动的分子机制以及此类应激源对整个群体的影响仍知之甚少。在此,我们比较了8个健康的风信子鹿角珊瑚群体与8个表现出通常与白色综合征相关的组织损失的群体的基因表达谱,所有样本均采集自帕劳附近的天然珊瑚礁环境。从患病珊瑚中采集了两种类型的组织:明显受影响的组织和看似健康的组织。
基于标签的RNA测序,随后进行加权基因共表达网络分析,确定了所有健康状态(疾病损伤、患病群体中看似健康的组织以及完全健康)之间共同调节的差异表达基因组。健康组织与患病组织之间的差异表明,几种先天免疫和组织修复途径被激活,同时钙化减少,并转向对储存脂质的代谢依赖。患病群体未受影响的部分,尽管显示出这些变化的趋势,但与完全健康的样本没有显著差异。尽管如此,网络分析确定了一组基因,提示免疫状态发生改变,这些基因在患病群体未受影响的部分中特异性上调。
完全健康的样本与患病群体中看似健康的部分相似,这表明白色综合征对风信子鹿角珊瑚的全身影响较弱,这意味着尽管患病,珊瑚群体在很大程度上仍能够维持其生理性能。在患病群体未受影响的部分中特异性上调的基因,可能与这些群体最初对自然发生的白色综合征的较高易感性有关,而不是疾病的结果。