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水稻突变体 X61 中光周期反应的完全丧失是由于光敏色素生色团生物合成基因的缺失所致。

Complete loss of photoperiodic response in the rice mutant line X61 is caused by deficiency of phytochrome chromophore biosynthesis gene.

机构信息

Graduate School of Agriculture, Kyoto University, Kitashirakawa, Sakyou, Kyoto, 606-8502, Japan.

出版信息

Theor Appl Genet. 2011 Jan;122(1):109-18. doi: 10.1007/s00122-010-1426-2. Epub 2010 Aug 11.

Abstract

In rice (Oryza sativa), a short-day plant, photoperiod is the most favorable external signal for floral induction because of the constant seasonal change throughout the years. Compared with Arabidopsis, however, a large part of the regulation mechanism of the photoperiodic response in rice still remains unclear due mainly to the lack of induced mutant genes. An induced mutant line X61 flowers 35 days earlier than its original variety Gimbozu under a natural photoperiod in Kyoto (35°01'N). We attempted to identify the mutant gene conferring early heading to X61. Experimental results showed that the early heading of X61 was conferred by a complete loss of photoperiodic response due to a novel single recessive mutant gene se13. This locus interacts with two crucial photoperiod sensitivity loci, Se1 and E1. Wild type alleles at these two loci do not function in coexistence with se13 in a homozygous state, suggesting that Se13 is an upstream locus of the Se1 and E1 loci. Linkage analysis showed that Se13 is located in a 110 kb region between the two markers, INDEL3735_1 and INDEL3735_3 on chromosome 1. A database search suggested that the Se13 gene is identical to AK101395 (=OsHY2), which encodes phytochromobilin synthase, a key enzyme in phytochrome chromophore biosynthesis. Subsequent sequence analysis revealed that X61 harbors a 1 bp insertion in exon 1 of OsHY2, which induces a frame-shift mutation producing a premature stop codon. It is therefore considered that the complete loss of photoperiodic response of X61 is caused by a loss of function of the Se13 (OsHY2) gene involved in phytochrome chromophore biosynthesis.

摘要

在水稻(Oryza sativa)中,作为短日照植物,光周期是花诱导最有利的外部信号,因为在每年的时间里都有持续的季节性变化。然而,与拟南芥相比,由于诱导突变基因的缺乏,水稻光周期反应调控机制的很大一部分仍然不清楚。一个诱导突变系 X61 在京都(35°01'N)的自然光照下比其原始品种 Gimbozu 早开花 35 天。我们试图鉴定赋予 X61 早期抽穗的突变基因。实验结果表明,X61 的早期抽穗是由于一个新的隐性单突变基因 se13 完全丧失光周期反应所致。该基因座与两个关键的光周期敏感性基因座 Se1 和 E1 相互作用。在纯合状态下,这些基因座的野生型等位基因不能与 se13 共存,表明 Se13 是 Se1 和 E1 基因座的上游基因座。连锁分析表明,Se13 位于染色体 1 上两个标记 INDEL3735_1 和 INDEL3735_3 之间的 110 kb 区域内。数据库搜索表明,Se13 基因与 AK101395(=OsHY2)相同,后者编码藻红胆素合酶,是藻胆色素生物合成中的关键酶。随后的序列分析表明,X61 在 OsHY2 的外显子 1 中含有 1 bp 的插入,导致移码突变并产生过早的终止密码子。因此,可以认为 X61 完全丧失光周期反应是由于参与藻胆色素生物合成的 Se13(OsHY2)基因失去功能所致。

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