Balachandran S., Osmond C. B., Makino A.
Department of Botany, Duke University, Durham, North Carolina 27708.
Plant Physiol. 1994 Mar;104(3):1043-1050. doi: 10.1104/pp.104.3.1043.
Photoacclimation was studied in tobacco leaves (Nicotiana tabacum cv Xanthi) infected with two strains of tobacco mosaic virus (TMV) and grown under different light and nitrogen nutrition regimes. Photosynthetic acclimation measured by the quantum yield and the maximum rate in saturating light of CO2-saturated photosynthesis was impaired to a greater extent in tobacco leaves infected with TMV strain PV230 than in those infected with TMV strain PV42. Infection with TMV strain PV230 severely impaired photosynthetic acclimation at high light/low nitrogen and during transfer from low to high light. Expanding leaves showing chlorotic-mosaic symptoms had greatly reduced capacity to acclimate to high light compared with controls and with developed leaves without visible symptoms. We conclude that the failure of expanding leaves to acclimate was largely due to the destruction of chloroplasts in yellow areas of the tissue, accompanied by severe reduction in ribulose-1,5-bisphosphate carboxylase/oxygenase levels, and corresponding reduction in photosynthesis on a leaf-area basis. When corrected for areas of healthy green tissue, photoacclimation of infected leaves was the same as that of controls. Visible symptom development was greatest in high light/low nitrogen treatments. In developed leaves without visible symptoms, virus accumulation, which was as extensive as in expanding leaves, accelerated senescence and impaired photoacclimation during transfer from low light to high light. Generally, infection with TMV strain PV42 did not impair photosynthetic acclimation and even enhanced it in some treatments, even though virus accumulated to the same concentration as in PV230-infected leaves. These data show that TMV does not simply impair photoacclimation in tobacco by competing with chloroplasts for leaf nitrogen reserves. Rather, specific properties of severe strains, such as PV230, which lead to visible symptom development and patchy loss of photosynthetic activity in expanding leaves as well as general acceleration of chloroplast senescence in developed leaves, contribute to impaired photoacclimation, which is generally exacerbated by low nitrogen nutrition.
在感染了两种烟草花叶病毒(TMV)毒株并在不同光照和氮营养条件下生长的烟草叶片(烟草品种Xanthi)中研究了光适应情况。通过量子产率和饱和光下二氧化碳饱和光合作用的最大速率来衡量的光合适应,在感染TMV毒株PV230的烟草叶片中比在感染TMV毒株PV42的叶片中受到的损害更大。感染TMV毒株PV230严重损害了高光/低氮条件下以及从低光向高光转变期间的光合适应。与对照以及没有可见症状的成熟叶片相比,出现褪绿花叶症状的伸展叶片适应高光的能力大大降低。我们得出结论,伸展叶片无法适应主要是由于组织黄色区域的叶绿体遭到破坏,同时1,5-二磷酸核酮糖羧化酶/加氧酶水平严重降低,以及基于叶面积的光合作用相应降低。当根据健康绿色组织的面积进行校正后,感染叶片的光适应与对照相同。可见症状在高光/低氮处理中最为明显。在没有可见症状的成熟叶片中,病毒积累与伸展叶片中一样广泛,加速了衰老并损害了从低光向高光转变期间的光适应。一般来说,感染TMV毒株PV42不会损害光合适应,甚至在某些处理中还会增强光合适应,尽管病毒积累到与感染PV230的叶片相同的浓度。这些数据表明,TMV并非简单地通过与叶绿体竞争叶片氮储备来损害烟草的光适应。相反,严重毒株(如PV230)的特定特性,导致伸展叶片出现可见症状和光合活性的斑块状丧失,以及成熟叶片中叶绿体衰老的普遍加速,这些都导致了光适应受损,而低氮营养通常会加剧这种情况。