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通过假定配体 CHALLAH 对气孔产生的区域特异性。

Regional specification of stomatal production by the putative ligand CHALLAH.

机构信息

Department of Biological Sciences, Stanford University, Stanford, CA 94305, USA.

出版信息

Development. 2010 Feb;137(3):447-55. doi: 10.1242/dev.040931. Epub 2010 Jan 7.

DOI:10.1242/dev.040931
PMID:20056678
Abstract

The problem of modulating cell fate programs to create distinct patterns and distributions of specialized cell types in different tissues is common to complex multicellular organisms. Here, we describe the previously uncharacterized CHALLAH (CHAL) gene, which acts as a tissue-specific regulator of epidermal pattern in Arabidopsis thaliana. Arabidopsis plants produce stomata, the cellular valves required for gas exchange, in virtually all aerial organs, but stomatal density and distribution differ among organs and along organ axes. Such regional regulation is particularly evident in plants mutant for the putative receptor TOO MANY MOUTHS (TMM), which produce excess stomata in leaves but no stomata in stems. Mutations in CHAL suppress tmm phenotypes in a tissue-specific manner, restoring stomatal production in stems while minimally affecting leaves. CHAL is similar in sequence to the putative stomatal ligands EPF1 and EPF2 and, like the EPFs, can reduce or eliminate stomatal production when overexpressed. However, CHAL and the EPFs have different relationships to TMM and the ERECTA (ER) family receptors. We propose a model in which CHAL and the EPFs both act through ER family receptors to repress stomatal production, but are subject to opposite regulation by TMM. The existence of two such ligand classes provides an explanation for TMM dual functionality and tissue-specific phenotypes.

摘要

调节细胞命运程序以在不同组织中创建不同类型的特化细胞的特定模式和分布是复杂多细胞生物的共同问题。在这里,我们描述了以前未表征的 CHALLAH(CHAL)基因,它作为拟南芥表皮模式的组织特异性调节剂。拟南芥植物在几乎所有的气生器官中产生气孔,这是气体交换所必需的细胞瓣膜,但气孔密度和分布在器官之间和器官轴上有所不同。这种区域调节在假定的受体 TOO MANY MOUTHS(TMM)突变体植物中尤为明显,TMM 突变体在叶片中产生过多的气孔,但在茎中没有气孔。CHAL 突变以组织特异性方式抑制 tmm 表型,在茎中恢复气孔产生,而对叶片的影响最小。CHAL 在序列上与假定的气孔配体 EPF1 和 EPF2 相似,并且与 EPFs 一样,当过度表达时可以减少或消除气孔的产生。然而,CHAL 和 EPFs 与 TMM 和 ERECTA(ER)家族受体的关系不同。我们提出了一个模型,其中 CHAL 和 EPFs 都通过 ER 家族受体起作用以抑制气孔产生,但受到 TMM 的相反调节。这两种配体类别的存在为 TMM 的双重功能和组织特异性表型提供了一个解释。

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