Terry MJ, Kendrick RE
School of Biological Sciences, University of Southampton, Bassett Crescent East, Southampton, SO16 7PX, United Kingdom (M.J.T.).
Plant Physiol. 1999 Jan;119(1):143-52. doi: 10.1104/pp.119.1.143.
The aurea (au) and yellow-green-2 (yg-2) mutants of tomato (Solanum lycopersicum L.) are unable to synthesize the linear tetrapyrrole chromophore of phytochrome, resulting in plants with a yellow-green phenotype. To understand the basis of this phenotype, we investigated the consequences of the au and yg-2 mutations on tetrapyrrole metabolism. Dark-grown seedlings of both mutants have reduced levels of protochlorophyllide (Pchlide) due to an inhibition of Pchlide synthesis. Feeding experiments with the tetrapyrrole precursor 5-aminolevulinic acid (ALA) demonstrate that the pathway between ALA and Pchlide is intact in au and yg-2 and suggest that the reduction in Pchlide is a result of the inhibition of ALA synthesis. This inhibition was independent of any deficiency in seed phytochrome, and experiments using an iron chelator to block heme synthesis demonstrated that both mutations inhibited the degradation of the physiologically active heme pool, suggesting that the reduction in Pchlide synthesis is a consequence of feedback inhibition by heme. We discuss the significance of these results in understanding the chlorophyll-deficient phenotype of the au and yg-2 mutants.
番茄(Solanum lycopersicum L.)的金黄色(au)和黄绿色-2(yg-2)突变体无法合成光敏色素的线性四吡咯发色团,导致植株呈现黄绿色表型。为了解这种表型的基础,我们研究了au和yg-2突变对四吡咯代谢的影响。由于原叶绿素酸酯(Pchlide)合成受到抑制,两个突变体的黑暗生长幼苗中Pchlide水平降低。用四吡咯前体5-氨基乙酰丙酸(ALA)进行的饲喂实验表明,au和yg-2中从ALA到Pchlide的途径是完整的,这表明Pchlide的减少是ALA合成受到抑制的结果。这种抑制与种子光敏色素的任何缺陷无关,并且使用铁螯合剂阻断血红素合成的实验表明,这两个突变都抑制了生理活性血红素池的降解,这表明Pchlide合成的减少是血红素反馈抑制的结果。我们讨论了这些结果在理解au和yg-2突变体叶绿素缺乏表型方面的意义。