gorgon, a novel missense mutation in the SHOOT MERISTEMLESS gene, impairs shoot meristem homeostasis in Arabidopsis.
gorgon, a novel missense mutation in the SHOOT MERISTEMLESS gene, impairs shoot meristem homeostasis in Arabidopsis.
复制标题
gorgon 是 SHOOT MERISTEMLESS 基因中的一种新型错义突变，会损害拟南芥中的芽分生组织稳态。
DOI：
10.1093/pcp/pcq028
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发表时间：
2010
影响因子：
4.9
通讯作者：
M. Aida
中科院分区：
文献类型：
--
作者：
S. Takano;Mitsuru Niihama;Harley M. Smith;M. Tasaka;M. Aida
芽分生组织是一组自我永存的细胞，最终产生植物的地上部分。拟南芥SHOOT MERISTEMLESS (STM)基因编码knotted1样同源盒转录因子，是芽分生组织形成和维持所必需的，该基因的功能丧失突变会导致芽分生组织完全丧失或过早终止。在这里，我们报告了 STM 的一个新的错义等位基因，gorgon (gor)，与已知的 stm 等位基因相比，它在芽分生组织缺陷方面表现出显着差异。 gor 表型是由同源结构域 53 位高度保守的精氨酸取代引起的，这对于其他同源结构域蛋白中的 DNA 结合很重要。在戈尔中，芽分生组织在胚胎后发育过程中不断增大，花分生组织经常发育出额外的轮生体。这些表型与分生组织标记表达域的扩大一起表明，该突变以与其他功能丧失等位基因相反的方向影响芽分生组织活性。然而，详细的遗传分析和过度表达研究表明，gor 代表一种新型的低等位基因，而不是表型所暗示的超等位基因。一致的是，gor等位基因严格需要功能性PENNYWISE（PNY）基因来维持芽分生组织活性，该基因编码已知的STM蛋白结合伴侣，而野生型等位基因即使在没有PNY的情况下也能有效维持分生组织。我们的结果表明同源结构域的 Arg53 在 STM 功能中起着关键作用，并且该残基的 gor 突变会损害芽分生组织稳态。
The shoot meristem is a group of self-perpetuating cells that ultimately gives rise to the aerial parts of plants. The Arabidopsis thaliana SHOOT MERISTEMLESS (STM) gene, which encodes a knotted1-like homeobox transcription factor, is required for shoot meristem formation and maintenance, and loss-of-function mutations in the gene result in complete loss or premature termination of the shoot meristem. Here, we report a novel missense allele of STM, gorgon (gor), which displays striking differences in shoot meristem defects compared with known stm alleles. The gor phenotype results from substitution of the highly conserved arginine at position 53 of the homeodomain, which is important for DNA binding in other homeodomain proteins. In gor, the shoot meristem enlarges continuously during post-embryonic development and the floral meristems frequently develop additional whorls. These phenotypes, together with enlarged expression domains of meristem markers, indicate that the mutation affects shoot meristem activity in the opposite direction to other loss-of-function alleles. However, detailed genetic analyses and overexpression studies indicate that gor represents a novel type of hypomorphic alleles rather than the hypermorph that is suggested by the phenotype. Consistently, the gor allele strictly requires the functional PENNYWISE (PNY) gene, which encodes a known binding partner of the STM protein, to maintain shoot meristem activity, whereas the wild-type allele efficiently maintains the meristem even in the absence of PNY. Our results suggest a critical role for Arg53 of the homeodomain in STM function and that the gor mutation at this residue impairs shoot meristem homeostasis.