Department of Plant Biology and Institute of Genomic Biology, University of Illinois, Urbana, IL, USA.
J Exp Bot. 2013 Jan;64(2):685-94. doi: 10.1093/jxb/ers364. Epub 2012 Dec 21.
Herbivory initiates a shift in plant metabolism from growth to defence that may reduce fitness in the absence of further herbivory. However, the defence-induced changes in carbon assimilation that precede this reallocation in resources remain largely undetermined. This study characterized the response of photosynthesis to herbivore induction of jasmonic acid (JA)-related defences in Nicotiana attenuata to increase understanding of these mechanisms. It was hypothesized that JA-induced defences would immediately reduce the component processes of photosynthesis upon attack and was predicted that wild-type plants would suffer greater reductions in photosynthesis than plants lacking JA-induced defences. Gas exchange, chlorophyll fluorescence, and thermal spatial patterns were measured together with the production of defence-related metabolites after attack and through recovery. Herbivore damage immediately reduced electron transport and gas exchange in wild-type plants, and gas exchange remained suppressed for several days after attack. The sustained reductions in gas exchange occurred concurrently with increased defence metabolites in wild-type plants, whereas plants lacking JA-induced defences suffered minimal suppression in photosynthesis and no increase in defence metabolite production. This suppression in photosynthesis occurred only after sustained defence signalling and defence chemical mobilization, whereas a short bout of feeding damage only transiently altered components of photosynthesis. It was identified that lipoxygenase signalling interacted with photosynthetic electron transport and that the resulting JA-related metabolites reduced photosynthesis. These data represent a metabolic cost to mounting a chemical defence against herbivory and link defence-signalling networks to the differential effects of herbivory on photosynthesis in remaining leaf tissues in a time-dependent manner.
食草作用会引发植物代谢从生长向防御的转变,如果没有进一步的食草作用,这可能会降低植物的适应性。然而,在资源重新分配之前,与防御相关的碳同化的防御诱导变化在很大程度上仍未确定。本研究的目的是描述拟南芥对茉莉酸(JA)相关防御的感应引起的光合作用对食草作用的响应,以增加对这些机制的理解。研究假设 JA 诱导的防御会立即减少攻击时光合作用的组成过程,并预测野生型植物的光合作用会比缺乏 JA 诱导的防御的植物受到更大的抑制。在攻击后和恢复期间,同时测量气体交换、叶绿素荧光和热空间模式,以及防御相关代谢产物的产生。食草动物的损害会立即降低野生型植物的电子传递和气体交换,并且在攻击后几天内气体交换仍会受到抑制。在野生型植物中,防御代谢物的持续增加与气体交换的持续减少同时发生,而缺乏 JA 诱导防御的植物的光合作用抑制最小,防御代谢物的产生也没有增加。这种光合作用的抑制仅在持续的防御信号和防御化学动员后发生,而短暂的摄食损伤仅会暂时改变光合作用的组成部分。研究确定了脂氧合酶信号与光合作用电子传递相互作用,并且由此产生的与 JA 相关的代谢物会降低光合作用。这些数据代表了对食草作用产生化学防御的代谢成本,并以时间依赖性的方式将防御信号网络与食草作用对剩余叶片组织中光合作用的差异影响联系起来。