Defects in CTP: PHOSPHORYLETHANOLAMINE CYTIDYLYLTRANSFERASE affect embryonic and postembryonic development in Arabidopsis
Defects in CTP: PHOSPHORYLETHANOLAMINE CYTIDYLYLTRANSFERASE affect embryonic and postembryonic development in Arabidopsis
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DOI：
10.1105/tpc.106.040840
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发表时间：
2006-12-01
期刊：
影响因子：
11.6
通讯作者：
Nishida, Ikuo
中科院分区：
文献类型：
--
作者：
Mizoi, Junya;Nakamura, Masanobu;Nishida, Ikuo
在拟南芥中使用TILLING策略（针对基因组中诱导的局部病变）分离编码CTP：磷酸化乙醇胺CYTIDYLYLTRANSFERASE （PECT; EC 2.7.7.14）的基因突变体，CTP：磷酸化乙醇胺CYTIDYLYLTRANSFERASE是磷脂酰乙醇胺生物合成中的限速酶。零突变pect1-6在八分期之前导致胚胎流产。然而，互交结果显示，pect1-6没有引起明显的配子体缺陷。在pect1-4， PECT活性下降了74%。尽管胚胎成熟延迟，生育能力降低，但这些突变体的生长一般正常。然而，在低温下，纯合子的果胶1-4植株表现出侏儒症。杂合子果胶1-6植株的PECT活性降低了47%，果胶1-4/果胶1-6 F1植株的PECT活性降低了80%，同时显示出磷脂酰乙醇胺含量虽小但显著降低，而磷脂酰胆碱含量则相互增加。野生型PECT1表达完全逆转了这些脂质变化。pect1-4/pect1-6 F1植株表现出严重的侏儒症、组织异常和低育性，部分原因是花药、胚胎和胚珠发育受到抑制，pect1-4幼苗的育性也降低了。诱导启动子控制下的PECT1 cDNA表达部分纠正了在PECT1 -4/ PECT1 -6 F1幼苗中观察到的突变表型，表明不同组织的故障对突变表型有协同作用。
A TILLING strategy ( for targeting-induced local-scale lesions in genomes) was used in Arabidopsis thaliana to isolate mutants of a gene encoding CTP: PHOSPHORYLETHANOLAMINE CYTIDYLYLTRANSFERASE (PECT; EC 2.7.7.14), a rate-limiting enzyme in phosphatidylethanolamine biosynthesis. A null mutation, pect1-6, caused embryo abortion before the octant stage. However, reciprocal crosses revealed that pect1-6 caused no significant gametophytic defect. In pect1-4, PECT activity was decreased by 74%. Growth was generally normal in these mutants, despite delays in embryo maturation and reduced fertility. At low temperatures, however, homozygotic pect1-4 plants displayed dwarfism. PECT activity was decreased by 47% in heterozygotic pect1-6 plants and by 80% in pect1-4/pect1-6 F1 plants, which also displayed a small but significant decrease of phosphatidylethanolamine and a reciprocal increase in phosphatidylcholine. These lipid changes were fully reversed by wild-type PECT1 expression. pect1-4/pect1-6 F1 plants displayed severe dwarfism, tissue abnormalities, and low fertility, which was attributable in part to inhibition of anther, embryo, and ovule development, as was the reduced fertility of pect1-4 seedlings. PECT1 cDNA expression under the control of an inducible promoter partially rectified the mutant phenotypes observed in pect1-4/pect1-6 F1 seedlings, indicating that malfunctions in different tissues have a synergistic effect on the mutant phenotypes.