HYDROXYPROLINE-RICH PROTEINS IN PLAGIOCHILA ARTICA LEAF DEVELOPMENT REGULATION

脯氨酰羟化酶拮抗剂的单独实验 并将其每种辅助底物/辅助因子提供给无菌 Plagiochila arctica (Hepaticae) 发育中植物的培养物 具有相同的结果：通常受到抑制的叶原基 在发展的早期阶段继续发展为 全尺寸的叶子。 由于脯氨酰羟化酶的功能 该系统是将哌啶基脯氨酸翻译后转化为 肽基-羟脯氨酸，我们初步得出结论，脯氨酰- 羟化酶抑制剂诱导的去抑制与改变有关 含羟脯氨酸的蛋白质（Hyp-蛋白质）的合成。 有两类 Hyp 蛋白广泛分布在绿色中 陆地植物，每种都含有不止一种“种类”的蛋白质。 两者都 P. arctica 中存在类，但数量 每个班级的代表尚不清楚。 我们在这里建议： 1. 找出每一类Hyp-蛋白的合成数量 北极原产地； 2. 更直接地检验假设 我们使用的脯氨酰羟化酶抑制剂实际上是有限的 P. arctica 中脯氨酸的翻译后羟基化；和 3. 使用免疫组织化学程序来关联 P. artica 中是否存在特定的 Hyp 蛋白 抑制/去抑制叶子发育。 这些细胞抑制/去抑制的研究 发育与几个基本的生物学问题有关。 首先， 哪些因素控制细胞增殖和细胞形状？ 其次，这些抑制作用在进化中发挥什么作用？ 改变表型发育？ 简而言之，我们看到的是 表型由基因型发展而来的生物化学。 当组织发生过程中发生抑制时， 器官发生或个体发育在很大程度上决定了大小。 哪里 相对于其他发展部分而言，抑制发生，它在很大程度上 决定形状。 是否发生或很大程度上抑制 决定增长和发展是否是“确定的”与 “不确定”，或“正常”与“异常”（病理性）。

Separate experiments in which antagonists of prolyl-hydroxylase and each of its cosubstrates/cofactors were supplied to axenic cultures of developing plants of Plagiochila arctica (Hepaticae) had the same result: leaf primordia that are normally suppressed at a very early stage of development continued to develop into full-sized leaves. Since the function of the prolyl-hydroxylase system is the posttranslational conversion of petidyl-proline to peptidyl-hydroxyproline, we tentatively conclude that prolyl- hydroxylase inhibitor-induced desuppression is related to altered synthesis of hydroxyproline-containing proteins (Hyp-proteins). There are two classes of Hyp-proteins widely distributed in green land plants, each with more than one "species" of protein. Both classes are represented in P. arctica, but the number of representatives of each class is not known yet. We propose here: 1. to find out how many Hyp-proteins of each class are synthesized in P. arctica; 2. to more directly test the assumption that the prolyl-hydroxylase inhibitors we used are in fact limiting posttranslational hydroxylation of proline in P. arctica; and 3. to use immunohistochemical procedures to correlate the presence/absence of specific Hyp-proteins identified in P. artica with suppression/desuppression of leaf development. These investigations of suppression/desuppression of cell development bear on several basic biological questions. First, what factors control cell multiplication and cell shape and secondly, what evolutionary role these suppressive effects play in altering phenotypic development? In short, we are seeing the biochemistry whereby phenotype develops from genotype. When suppression occurs during the course of histogenesis, organogenesis or ontogeny largely determines size. Where suppression occurs relative to other developing parts, it largely determines shape. Whether suppression occurs or nor largely determines whether growth and development will be "determinate" vs "indeterminate", or "normal" vs "abnormal" (pathological).