Sucrose prevents up-regulation of senescence-associated genes in carnation petals

Sucrose prevents up-regulation of senescence-associated genes in carnation petals
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DOI:
10.1093/jxb/erm076
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发表时间:
2007-09-01
影响因子:
6.9
通讯作者:
van Wordragen, Monique F.
van Wordragen, Monique F.
中科院分区:
生物学1区
文献类型:
--
作者:
Hoeberichts, Frank A.;van Doorn, Wouter G.;van Wordragen, Monique F.

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使用 cDNA 微阵列来表征康乃馨(石竹)切花花瓣中与衰老相关的基因表达,这些花瓣是从开花期到第一个衰老症状期间取样的。使用消减杂交,在这些微阵列上点样的 PCR 片段群富集了花特异性和衰老特异性基因。大约 90% 的转录本显示数量大幅增加,大约 25% 是短暂增加,大约 65% 在整个 7 天的实验中增加。硫代硫酸银(STS)治疗可以阻断乙烯受体并防止正常的衰老症状,从而阻止了几乎所有这些基因的上调。蔗糖处理也显着延迟了可见的衰老。它对基因表达的影响与 STS 非常相似,表明可溶性糖充当乙烯信号转导的阻遏物。分离出两个编码康乃馨 EIN3 样 (EIL) 蛋白的片段,其中一些是控制乙烯反应基因的关键转录因子。其中之一 (Dc-EIL3) 在衰老过程中上调。它的上调被STS延迟并被蔗糖阻止。因此,蔗糖似乎部分通过阻止 Dc-EIL3 的上调来抑制乙烯信号传导。其他一些转录因子表现出转录本丰度的早期增加:MYB 样 DNA 结合蛋白、MYC 蛋白、MADS-box 因子和锌指蛋白。表明在乙烯以外的激素衰老中起作用的基因编码了 Aux/IAA 蛋白(调节生长素诱导基因的转录)和细胞分裂素氧化酶/脱氢酶(降解细胞分裂素)。总而言之,这些结果表明衰老过程中存在一个主开关,控制着众多乙烯反应基因的协调上调。 Dc-EIL3 可能是该主交换机(的一部分)。
cDNA microarrays were used to characterize senescence-associated gene expression in petals of cut carnation (Dianthus caryophyllus) flowers, sampled from anthesis to the first senescence symptoms. The population of PCR fragments spotted on these microarrays was enriched for flower-specific and senescence-specific genes, using subtractive hybridization. About 90% of the transcripts showed a large increase in quantity, approximately 25% transiently, and about 65% throughout the 7 d experiment. Treatment with silver thiosulphate (STS), which blocks the ethylene receptor and prevented the normal senescence symptoms, prevented the up-regulation of almost all of these genes. Sucrose treatment also considerably delayed visible senescence. Its effect on gene expression was very similar to that of STS, suggesting that soluble sugars act as a repressor of ethylene signal transduction. Two fragments that encoded a carnation EIN3-like (EIL) protein were isolated, some of which are key transcription factors that control ethylene response genes. One of these (Dc-EIL3) was up-regulated during senescence. Its up-regulation was delayed by STS and prevented by sucrose. Sucrose, therefore, seems to repress ethylene signalling, in part, by preventing up-regulation of Dc-EIL3. Some other transcription factors displayed an early increase in transcript abundance: a MYB-like DNA binding protein, a MYC protein, a MADS-box factor, and a zinc finger protein. Genes suggesting a role in senescence of hormones other than ethylene encoded an Aux/IAA protein, which regulate transcription of auxin-induced genes, and a cytokinin oxidase/dehydrogenase, which degrades cytokinin. Taken together, the results suggest a master switch during senescence, controlling the co-ordinated up-regulation of numerous ethylene response genes. Dc-EIL3 might be (part of) this master switch.