MOLECULAR MECHANISMS ON THE REVERSIBLE MICROBODY TRANITION

在南瓜和拟南芥等脂肪幼苗的子叶中，微体在绿化过程中由乙氧体向叶片过氧体转变。在子叶衰老过程中，乙醛酶体向叶片过氧化物酶体的反向转变发生。研究表明，glyoxysomes与叶片过氧化物酶体之间的功能转换受到基因表达、蛋白质易位和蛋白质降解等多个层面的控制。遗传学方法可能是在分子水平上理解微体转变背后的调控机制的有效策略。我们筛选了2,4-二hiorophenoxybutyric acid （2,4- db）抗性突变体，这些突变体在glyoxysomal功能上存在缺陷。先前已经证明2,4- db在高等植物中通过乙氧体脂肪酸β-氧化作用代谢产生除草剂。为了分离glyoxysomal fatty acid β-oxidation有缺陷的突变体，对拟南芥（Arabidopsis .）的突变系进行了筛选，使其在毒性水平为2,4- db的条件下生长。12个突变体存活了下来，其中4个需要蔗糖来促进发芽后的生长。这一结果表明，这些突变体在乙醛酶体脂肪酸β-氧化方面存在缺陷，因为乙醛酶体脂肪酸β-氧化在萌发过程中将储存脂转化为蔗糖的过程中起重要作用。其中一个突变体缺乏硫酶蛋白，这是一种在萌发和随后的幼苗生长过程中参与脂肪酸β氧化的酶。另一个突变体在细胞内从细胞质到乙氧基体的硫硫酶运输上有缺陷。两种突变体的黄化子叶都有形态异常的乙氧化酶体。在巯基酶缺陷突变体中，乙醛酶体具有管状结构，其中含有许多囊泡。通过对突变体的电镜分析，研究了脂肪酸β氧化过程中脂质体与脂质体之间的相互作用以及脂质体向脂质体的转运。少

In cotyledons of some fatty seedlings such as pumpkin and Arabidopsis, microbody transition from glyoxysomes to leaf peroxysomes is observed during greening. Reverse transition from glyoxysomes to leaf peroxisomes occurs during senescence of the cotyledons. It has been suggested that the functional conversion between glyoxysomes and leaf peroxisomes is controlled at various levels, such as gene expression, protein translocation and protein degradation. A genetically approach may be an effective strategy toward understanding the regulatory mechanism(s) underlying the microbody transition at the molecular level. We screened 2,4-dichIorophenoxybutyric acid (2,4-DB)-resistant mutants that have defects in glyoxysomal function.It has been previously demonstrated that 2,4-DB is metabolized to produce a herbicide, by the action of glyoxysomal fatty acid β-oxidation in higher plants. In order to isolate mutants that have defects in glyoxysomal fatty acid β-oxidation, mutant lines of Arabidopsis … More seedlings were screened for growth in the presence of toxic levels of 2,4-DB. Twelve of the mutants survived and of these, four required sucrose for post-germinative growth. This result suggests that these mutants have defects in glyoxysomal fatty acid β-oxidation, since glyoxysomal fatty acid β-oxidation has an important role in converting sucrose from storage lipids during germination. One of the mutants lacks thiolase protein, an enzyme involved in fatty acid β-oxidation during germination and subsequent seedling growth. Another mutant has a defect in the intracellular transport of thiolase form the cytosol to glyoxysomes. Etiolated cotyledons of both mutants have glyoxysomes with abnormal morphology. In the thiolase defective mutants, glyoxysomes have tubular structures that contain many vesicles. Interaction between glyoxysomes and lipid bodies and the transport of lipids from lipid bodies to glyoxysomes during fatty acid β-oxidation are studied by using the electron microscopic analysis of the mutants. Less