The role of the ribosome in plant development

生命是通过一系列核心事件维持的：dna - mrna -蛋白质。任何生物体要分裂、生长、发育和分化，导致蛋白质合成的一系列事件都需要受到调节。存在多种机制来帮助确定单个细胞中每种蛋白质的产生时间、地点和数量。调节蛋白质生产的一种方法是控制读取mRNA的机器，并从基本氨基酸构建块中构建蛋白质。这个了不起的机器就是核糖体。核糖体由一个小亚基和一个大亚基组成，共由3个RNA分子和近80种蛋白质组成。作为筛选控制叶片发育的基因的一部分，我们已经分离出大亚基和小亚基核糖体蛋白的突变。这些突变体被称为背驮式突变体（pgy），令人惊讶的是，当它们与叶片发育突变体不对称叶片1 （as1）结合时，会产生一种非常特殊的发育缺陷。as1pgy双突变体具有引人注目的表型，其中叶子从其他叶子的表面长出来。然而，pgy突变体本身对植物发育的影响很小。as1pgy双突变体的发育表型表明，只有选定的靶转录物对核糖体蛋白功能的丧失更敏感。这些靶标可能是什么？为什么它们对核糖体蛋白损失敏感？我们有几个可测试的模型来解决这些重要的问题。一种可能性是核糖体的一个子集与其他蛋白质相互作用，正是这个子集受到pgy突变的影响。另一种可能性是一些转录本中的序列对pgy突变很敏感。拟南芥的每个核糖体蛋白都有几个基因，所以第三种可能性是，一个家族中的核糖体蛋白并不是都在做同样的事情。在这种情况下，携带不同家族成员的核糖体功能不同。我们正在使用遗传学和生物化学来测试这些模型，并找出PGY基因突变产生特定表型的原因以及PGY基因如何起作用。例如，一个目标是确定直接靶基因。找到一个直接的靶标将使我们能够操纵可能对核糖体功能敏感的靶标的序列特征。我们还可以用遗传学来比较基因家族中核糖体蛋白的功能，看看它们是相同的还是不同的。有了这些实验的结果，我们可以开始解决核糖体控制基因表达的机制。

Life is maintained through a central chain of events: DNA-mRNA-protein. For any organism to divide, grow, develop and differentiate the chain of events leading to protein synthesis needs to be regulated. Multiple mechanisms exist to help achieve when, where and how much of each protein in an individual cell is produced. One way to regulate protein production is to control the machine that reads mRNA and builds proteins from the basic amino acid building blocks. This remarkable machine is the ribosome. The ribosome is composed of a small and a large subunit, together consisting of 3 RNA molecules and nearly 80 proteins. As part of a screen to find genes controlling leaf development we have isolated mutations in large and small subunit ribosomal proteins. These mutants are called piggyback (pgy) and, surprisingly, they produce a very specific developmental defect when combined with the leaf development mutant asymmetric leaves1 (as1). as1 pgy double mutants have a dramatic phenotype where leaves grow out from the surface of other leaves. However, by themselves pgy mutants have very little effect on plant development. The developmental phenotype of as1 pgy double mutants indicates only selected target transcripts are more sensitive to loss of ribosomal protein function. What might these targets be and why are they sensitive to ribosomal protein loss? We have several testable models to address these important questions. One possibility is that a subset of ribosomes interacts with other proteins and it is this subset that is affected by pgy mutations. Another possibility is that sequences in some transcripts are sensitive to pgy mutations. Arabidopsis has several genes for each ribosomal protein so a third possibility is that ribosomal proteins within a family are not all doing the same thing. In this case ribosomes carrying different family members are functionally different. We are using genetics and biochemistry to test these models and find out why mutations in PGY genes produce a specific phenotype and how PGY genes might work. For instance one goal is to identify direct target genes. Finding a direct target will enable us to manipulate sequence features of the target that may be sensitive to ribosome function. We can also use genetics to compare the function of ribosomal proteins within a gene family to see if they are the same or different. With the results of these experiments we can start to address the mechanism by which the ribosome controls gene expression.