Molecular genetic analyses of the plant shoot formation using Arabidopsis mutants.

在先前的研究中，ACL 5基因（拟南芥精胺合酶的编码基因）的功能缺失突变已被证明会导致严重的矮化表型。为了进一步了解多胺在植物中的功能，对精脒和精胺合成缺陷突变体进行了鉴定。拟南芥基因组有两个亚精胺合酶基因，SPDS 1和SPDS 2，以及两个精胺合酶基因，ACL 5和SPMS。发现SPDS 1、SPDS 2双突变体是胚胎致死的，这表明亚精胺对于植物的存活是必需的，而ACL 5 -1、SPMS-1双突变体与野生型完全一样有活力，并且除了由于ACL 5 -1而导致的茎生长减少之外，没有表现出表型。为了阐明精胺在植物芽发育中作用模式的分子基础，从acl 5纯合植株中分离到抑制acl 5矮化表型的acl 5抑制子（Suppressor of acl 5，Sac）突变体。到目前为止，已经发现了四种突变。精细定位和DNA序列测定结果表明，Sac 51 -1等位基因编码一个转录因子的基因上游ORF（uORF）发生了点突变，同时还分离到了短茎和中脉（ssm）突变体，该突变体具有半矮秆和波形叶两种表型。图位克隆的基因是有缺陷的ssm突变体中发现了一个小的缺失，在第6内含子的基因编码的syntaxin，VAM 3/SYP 22，这已经牵连在小泡运输到液泡。

In a previous study, loss-of-function mutations of the ACL5 gene, which encodes spermine synthase in Arabidopsis thaliana, have been shown to result in a severely dwarfed phenotype. To know further the function of polyamines in plants, mutants defective in the synthesis of spermidine and spermine were characterized. The Arabidopsis genome has two genes for spermidine synthase, SPDS1 and SPDS2, and two for spermine synthase, ACL5 and SPMS. spds1 spds2 double mutants were found to be embryonic lethal, suggesting that spermidine is essential for survival of plants, while acl5-1 spms-1 double mutants are fully as viable as the wild type and show no phenotype except for the reduced stem growth due to acl5-1. This suggests that ACL5 and SPMS function in different aspects of the plant growth.To elucidate the molecular basis of the mode of actions of spermine in plant shoot development, Suppressor of acl5 (Sac) mutants were isolated from homozygous acl5 plants as mutants that suppress the dwarfed phenotype of acl5. So far, four mutations have been identified. Fine mapping experiments and DNA sequence determination revealed that the Sac51-1 allele contains a point mutation in an upstream ORF (uORF) of a gene encoding a putative transcription factor.On the other hand, the short stem and midrib (ssm) mutants showing both semi-dwarf and wavy leaf phenotypes were isolated and characterized. Map-based cloning of the gene that is defective in ssm mutants has uncovered a small deletion in the 6th intron of a gene encoding a syntaxin, VAM3/SYP22, which has been implicated in vesicle transport to the vacuole.