Adenosine kinase deficiency is associated with developmental abnormalities and reduced transmethylation
Adenosine kinase deficiency is associated with developmental abnormalities and reduced transmethylation
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DOI：
10.1104/pp.010880
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发表时间：
2002-03-01
期刊：
影响因子：
7.4
通讯作者：
Wagner, C
中科院分区：
文献类型：
--
作者：
Moffatt, BA;Stevens, YY;Wagner, C
腺苷（Ado）激酶（ADK; ATP：Ado 5'磷酸转移酶，EC 2.7.1.20）催化从Ado和ATP补救合成腺嘌呤一磷酸。在拟南芥中，ADK由两个cDNA编码，这两个cDNA具有89%的核苷酸同一性，并且在叶、茎、根和花中组成性但差异性地表达。为了研究ADK在植物代谢中的规律，已经通过ADK 1 cDNA的正义和反义表达创建了这种酶活性缺陷的株系。这些品系中ADK活性的水平范围为野生型拟南芥中发现的活性的7%至70%。具有50%或更多野生型活性的转基因植物具有正常形态。相比之下，具有小于10%ADK活性的植物较小，具有圆形、波浪形的叶和紧凑、浓密的外观。由于初生T枝缺乏伸长，角果从莲座丛成簇延伸。FuriilitN减少是因为雄蕊丝不能正常伸长;下胚轴和根的伸长也减少。由S-腺苷-L-甲硫氨酸（SAM）依赖的甲基化反应产生的S-腺苷-L-高-半胱氨酸（SAH）的水解是植物中Ado的关键来源。ADK缺陷系中Ado补救的缺乏导致SAH水平的增加并导致SAM依赖性转甲基化的抑制。ADK活性和种子粘液中甲酯化果胶的水平之间存在直接相关性，如通过钌红染色、免疫荧光标记或直接测定所监测的。这些结果表明，Ado必须被ADK稳定地去除，以防止SAH水解酶的反馈抑制，并维持SAM的利用和再循环。
Adenosine (Ado) kinase (ADK; ATP:Ado 5' phosphotransferase, EC 2.7.1.20) catalyzes the salvage synthesis of adenine monophosphate from Ado and ATP. In Arabidopsis, ADK is encoded by two CDNAs that share 89% nucleotide identity and are constitutively, yet differentially, expressed in leaves, stems, roots, and flowers. To investigate the rule of ADK in plant metabolism, lines deficient in this enzyme activity have been created by sense and antisense expression of the ADK1 cDNA. The levels of ADK activity in these lines range from 7% to 70% of the activity found in wild-type Arabidopsis. Transgenic plants with 50% or more of the wild-type activity have a normal morphology. In contrast, plants with less than 10% ADK activity are small with rounded, wavy leaves and a compact, bushy appearance. Because of the lack of elongation of the primar T shoot, the siliques extend in a cluster from the rosette. FuriilitN is decreased because the stamen filaments do not elongate normally; hypocotyl and root elongation are reduced also, The hydrolysis of S-adenosyl-L-homo-cysteine (SAH) produced from S-adenosyl-L-methionine (SAM)-dependent methylation reactions is a key source of Ado in plants. The lack of Ado salvage in the ADK-deficient lines leads to an increase in the SAH level and results in the inhibition of SAM-dependent transmethylation. There is a direct correlation between ADK activity and the level of methylesterified pectin in seed mucilage, as monitored by staining with ruthenium red, immunofluorescence labeling, or direct assay. These results indicate that Ado must be steadily removed by ADK to prevent feedback inhibition of SAH hydrolase and maintain SAM utilization and recycling.