Seaton G G, Hurry V M, Rohozinski J
Research School of Biological Sciences, Institute of Advanced Studies, Australian National University, Canberra, Australia.
FEBS Lett. 1996 Jul 8;389(3):319-23. doi: 10.1016/0014-5793(96)00615-1.
In higher plants non-photochemical dissipation of excess light, trapped by the pigment pool of photosystem II, prevents photodamage to the photosynthetic apparatus. We report here that an algal virus infecting Chlorella strain Pbi induces non-photochemical quenching of photosystem II fluorescence, indicating enhanced loss of absorbed light energy from photosystem II. This phenomenon occurs soon after the establishment of the virus infection cycle and is observed at low irradiance (20 micromol quanta m-2 s-1). At low light, infection associated non-photochemical quenching is not linked to extensive conversion of violaxanthin to antheraxanthin and zeaxanthin. However, such conversion occurs rapidly (2-10 min) in infected cells under conditions of high irradiance (100-300 micromol quanta m-2 s-1). Under similar conditions uninfected Chlorella cells do not display significant changes in non-photochemical quenching.
在高等植物中，光合系统II色素库捕获的过量光能的非光化学耗散可防止光合装置受到光损伤。我们在此报告，一种感染小球藻Pbi菌株的藻类病毒会诱导光合系统II荧光的非光化学猝灭，这表明光合系统II吸收的光能损失增加。这种现象在病毒感染周期建立后不久就会出现，并且在低光照强度（20微摩尔光子·米⁻²·秒⁻¹）下也能观察到。在低光照条件下，与感染相关的非光化学猝灭与紫黄质向花药黄质和玉米黄质的大量转化无关。然而，在高光照强度（100 - 300微摩尔光子·米⁻²·秒⁻¹）条件下，受感染细胞中这种转化会迅速发生（2 - 10分钟）。在类似条件下，未感染的小球藻细胞在非光化学猝灭方面没有显著变化。
