Strigolactone signaling regulates rice leaf senescence in response to a phosphate deficiency
Strigolactone signaling regulates rice leaf senescence in response to a phosphate deficiency
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DOI：
10.1007/s00425-014-2096-0
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发表时间：
2014-06
期刊：
影响因子：
4.3
通讯作者：
Y. Yamada;Soya Furusawa;Seiji Nagasaka;K. Shimomura;Shinjiro Yamaguchi;Mikihisa Umehara
中科院分区：
文献类型：
--
作者：
Y. Yamada;Soya Furusawa;Seiji Nagasaka;K. Shimomura;Shinjiro Yamaguchi;Mikihisa Umehara
独脚金内酯（SL）作为植物激素，抑制芽分枝并刺激茎的次生生长、主根生长和根毛伸长。在藓类植物小立碗藓中，SL调节绿丝分枝和菌落扩展。此外，SL-缺陷和SL-不敏感的突变体表现出延迟叶片衰老。为探讨SL对水稻叶片衰老的影响，我们用合成的SL类似物GR 24处理水稻突变体的叶段，并评估它们的叶绿素含量、离子渗漏和衰老相关基因的表达水平。外源施加GR 24恢复正常叶片衰老SL缺陷突变体，但不是在SL不敏感的突变体。大多数植物在缺磷时会大量产生内源SL。因此，我们评估了GR 24在磷酸盐缺乏下的作用。叶绿素水平没有不同的野生型之间的充足和缺乏磷酸盐的条件下，但增加在SL-缺乏突变体磷酸盐缺乏，导致在强烈促进叶片衰老的GR 24治疗。这些结果表明，突变体在磷酸盐缺乏下表现出对GR 24的响应性增加。此外，GR 24加速叶片衰老在完整的SL-缺陷突变体在磷缺乏以及黑暗诱导的叶片衰老。GR 24对10号的作用强于17号。基于这些结果，我们认为SL调节叶片衰老响应磷酸盐缺乏。
Strigolactones (SLs) act as plant hormones that inhibit shoot branching and stimulate secondary growth of the stem, primary root growth, and root hair elongation. In the mossPhyscomitrella patens, SLs regulate branching of chloronemata and colony extension. In addition, SL-deficient and SL-insensitive mutants show delayed leaf senescence. To explore the effects of SLs on leaf senescence in rice (Oryza sativaL.), we treated leaf segments of ricedwarfmutants with a synthetic SL analogue, GR24, and evaluated their chlorophyll contents, ion leakage, and expression levels of senescence-associated genes. Exogenously applied GR24 restored normal leaf senescence in SL-deficient mutants, but not in SL-insensitive mutants. Most plants highly produce endogenous SLs in response to phosphate deficiency. Thus, we evaluated effects of GR24 under phosphate deficiency. Chlorophyll levels did not differ of in the wild-type between the sufficient and deficient phosphate conditions, but increased in the SL-deficient mutants under phosphate deficiency, leading in the strong promotion of leaf senescence by GR24 treatment. These results indicate that the mutants exhibited increased responsiveness to GR24 under phosphate deficiency. In addition, GR24 accelerated leaf senescence in the intact SL-deficient mutants under phosphate deficiency as well as dark-induced leaf senescence. The effects of GR24 were stronger ind10compared tod17. Based on these results, we suggest that SLs regulate leaf senescence in response to phosphate deficiency.