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

在之前的一项研究中，编码拟南芥精胺合成酶的ACL5基因的功能缺失突变已被证明会导致严重的侏儒表型。为了进一步了解多胺在植物中的功能，对合成亚精胺和精胺缺陷的突变体进行了表征。拟南芥基因组有两个精胺合成酶基因SPDS1和SPDS2，两个精胺合成酶基因ACL5和SPMS。Spds1 spds2双突变体具有胚胎致死性，表明亚精胺对植物的生存至关重要，而acl5-1 spms-1双突变体与野生型一样具有完全的存活率，除了由于acl5-1导致茎生长减少外，没有表现出任何表型。这表明ACL5和SPMS在植物生长的不同方面起作用。为了阐明精胺在植物茎部发育中的作用模式的分子基础，从纯合子acl5植株中分离出acl5的Suppressor （Sac）突变体，作为抑制acl5矮化表型的突变体。到目前为止，已经发现了四种突变。精细的定位实验和DNA序列测定显示，Sac51-1等位基因在编码一个假定的转录因子的基因的上游ORF （uORF）中含有一个点突变。另一方面，短茎和中脉（ssm）突变体具有半矮秆和波浪叶表型，并进行了分离和鉴定。图谱克隆ssm突变体基因缺陷的发现了一个小删除6号内含子的基因编码一个突触融合蛋白,VAM3 / SYP22,已与囊泡运输到液泡。

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.