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缺陷内核1促进并维持植物表皮分化。

DEFECTIVE KERNEL 1 promotes and maintains plant epidermal differentiation.

作者信息

Galletti Roberta, Johnson Kim L, Scofield Simon, San-Bento Rita, Watt Andrea M, Murray James A H, Ingram Gwyneth C

机构信息

Laboratoire de Reproduction et Développement des Plantes, Ecole Normale Supérieure de Lyon, 46 allée d'Italie, Lyon 69364, Cedex 07, France

ARC Centre of Excellence in Plant Cell Walls, School of Botany, University of Melbourne, Royal Parade, Parkville, Victoria 3010, Australia.

出版信息

Development. 2015 Jun 1;142(11):1978-83. doi: 10.1242/dev.122325. Epub 2015 May 7.

Abstract

During plant epidermal development, many cell types are generated from protodermal cells, a process requiring complex co-ordination of cell division, growth, endoreduplication and the acquisition of differentiated cellular morphologies. Here we show that the Arabidopsis phytocalpain DEFECTIVE KERNEL 1 (DEK1) promotes the differentiated epidermal state. Plants with reduced DEK1 activity produce cotyledon epidermis with protodermal characteristics, despite showing normal growth and endoreduplication. Furthermore, in non-embryonic tissues (true leaves, sepals), DEK1 is required for epidermis differentiation maintenance. We show that the HD-ZIP IV family of epidermis-specific differentiation-promoting transcription factors are key, albeit indirect, targets of DEK1 activity. We propose a model in which DEK1 influences HD-ZIP IV gene expression, and thus epidermis differentiation, by promoting cell adhesion and communication in the epidermis.

摘要

在植物表皮发育过程中,许多细胞类型由原表皮细胞产生,这一过程需要细胞分裂、生长、核内复制以及分化细胞形态的获得之间进行复杂的协调。我们在此表明,拟南芥植物钙蛋白酶缺陷型内核1(DEK1)促进表皮分化状态。尽管DEK1活性降低的植物表现出正常的生长和核内复制,但它们产生的子叶表皮具有原表皮特征。此外,在非胚胎组织(真叶、萼片)中,DEK1是维持表皮分化所必需的。我们表明,表皮特异性分化促进转录因子的HD-ZIP IV家族是DEK1活性的关键间接靶标。我们提出了一个模型,其中DEK1通过促进表皮中的细胞粘附和通讯来影响HD-ZIP IV基因表达,从而影响表皮分化。

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