DDB1 complexes in arabidopsis visible and UV light response

植物对光很敏感。当在黑暗中生长时，比如在岩石或木板下，植物幼苗又高又细，颜色苍白，叶子紧闭。豆芽就是这种生长方式的一个例子。当植物在阳光下生长时，虽然它们又短又绿，叶子张开以吸收阳光。我们对拟南芥的研究集中在一个突变体上，det1，它在这个过程中有缺陷——即使在黑暗中生长，它看起来也像一个光生长的植物。这表明DET1通常是植物对光反应的重要组成部分。我们正试图理解DET1是如何发挥这一作用的。我们发现DET1蛋白与一种叫做受损dna结合蛋白1 （DDB1）的蛋白相互作用。DDB1最初是在人类中发现的，它参与了紫外线损伤DNA的修复。DDB1活性在一些人类色素性干皮病患者中存在缺陷。这些人有患皮肤癌的风险，因为他们无法修复紫外线造成的DNA损伤。我们的结果非常令人兴奋，因为它表明，可能存在一种共同的机制来应对“好”光，它使植物生长，而“坏”紫外线，它对所有生命形式都有害。我们希望通过对DET1和DDB1的研究，帮助设计出具有最佳光响应和抗紫外线能力的作物植株。

Plants are very sensitive to light. When grown in the dark, such as under a rock or board, plant seedlings are tall, thin, pale, and keep their leaves closed. Bean sprouts are an example of this type of growth. When plants grow in the light though they are short and green with leaves open to absorb the sunlight. Our studies in the mustard relative Arabidopsis have centred around a mutant, det1, that is defective in this process - it looks like a light-grown plant even when grown in the dark. This suggests that DET1 is normally an important part of how the plant responds to light. We are trying to understand how DET1 performs this role. We have found that the DET1 protein interacts with a protein called Damaged DNA-Binding protein 1 (DDB1). DDB1 was originally identified in humans, where it is involved in the repair of UV-damaged DNA. DDB1 activity is defective in some human xeroderma pigmentosa patients. These people are at risk for skin cancer because they are unable to repair DNA damage caused by UV light. Our result is very exciting because it suggests that there may be a common mechanism of responding to "good" light, which makes plants grow, and "bad" UV light, which is damaging to all life forms. We hope by studying DET1 and DDB1 to help design crop plants with both optimal light response and UV protective capacity.