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Effect of CO2-induced seawater acidification on growth photosynthesis and inorganic carbon acquisition of the harmful bloom-forming marine microalga Karenia mikimotoi

机译:CO2诱导的海水酸化对有害形成水华的海洋微藻(Karenia mikimotoi)生长光合作用和无机碳吸收的影响

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摘要

Karenia mikimotoi is a widespread, toxic and non-calcifying dinoflagellate, which can release and produce ichthyotoxins and hemolytic toxins affecting the food web within the area of its bloom. Shifts in the physiological characteristics of K. mikimotoi due to CO2-induced seawater acidification could alter the occurrence, severity and impacts of harmful algal blooms (HABs). Here, we investigated the effects of elevated pCO2 on the physiology of K. mikimotoi. Using semi-continuous cultures under controlled laboratory conditions, growth, photosynthesis and inorganic carbon acquisition were determined over 4–6 week incubations at ambient (390ppmv) and elevated pCO2 levels (1000 ppmv and 2000 ppmv). pH-drift and inhibitor-experiments suggested that K. mikimotoi was capable of acquiring HCO3-, and that the utilization of HCO3- was predominantly mediated by anion-exchange proteins, but that HCO3- dehydration catalyzed by external carbonic anhydrase (CAext) only played a minor role in K. mikimotoi. Even though down-regulated CO2 concentrating mechanisms (CCMs) and enhanced gross photosynthetic O2 evolution were observed under 1000 ppmv CO2 conditions, the saved energy did not stimulate growth of K. mikimotoi under 1000 ppmv CO2, probably due to the increased dark respiration. However, significantly higher growth and photosynthesis [in terms of photosynthetic oxygen evolution, effective quantum Yield (Yield), photosynthetic efficiency (α), light saturation point (Ek) and ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) activity] were observed under 2000 ppmv CO2 conditions. Furthermore, elevated pCO2 increased the photo-inhibition rate of photosystem II (β) and non-photochemical quenching (NPQ) at high light. We suggest that the energy saved through the down-regulation of CCMs might lead to the additional light stress and photo-damage. Therefore, the response of this species to elevated CO2 conditions will be determined by more than regulation and efficiency of CCMs.
机译:米氏卡伦氏菌是一种广泛的,有毒的,非钙化的鞭毛藻,可以释放并产生鱼腥毒素和溶血毒素,影响其开花区域的食物网。由于CO2诱导的海水酸化而引起的K. mikimotoi生理特征的变化可能会改变有害藻华(HABs)的发生,严重程度和影响。在这里,我们调查了升高的pCO2对K. ​​mikimotoi生理的影响。在受控的实验室条件下使用半连续培养,在环境温度(390ppmv)和升高的pCO2水平(1000 ppmv和2000 ppmv)下孵育4-6周确定了生长,光合作用和无机碳的获取。 pH漂移和抑制剂实验表明,三本K.能够获得HCO3 -,并且HCO3 -的利用主要是由阴离子交换蛋白介导的,但是外部碳酸酐酶(CAext)催化的HCO3 -脱水仅在mikimotoi K. mikimotoi中起较小的作用。即使在1000 ppmv CO2条件下观察到下调的CO2浓缩机制(CCM)和增强的总光合作用O2释放,但节省的能量并不能刺激在1000 ppmv CO2下的K. mikimotoi的生长,这可能是由于暗呼吸增加所致。但是,其生长和光合作用明显更高[就光合作用的氧气释放,有效量子产率(Yield),光合作用效率(α),光饱和点(Ek)和核糖-1,5-双磷酸羧化酶/加氧酶(Rubisco)活性而言]在2000 ppmv CO2条件下观察到。此外,pCO2的升高会增加强光下光系统II(β)和非光化学猝灭(NPQ)的光抑制率。我们建议通过下调CCM节省的能量可能会导致额外的光应力和光损伤。因此,该物种对升高的CO2条件的响应将不仅由CCM的调节和效率决定。

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