Cell cycle regulates cell type in the Arabidopsis sepal

Development (Impact Factor: 6.27). 10/2012; 139(23). DOI: 10.1242/dev.082925
Source: PubMed

ABSTRACT The formation of cellular patterns during development requires the coordination of cell division with cell identity specification. This coordination is essential in patterning the highly elongated giant cells, which are interspersed between small cells, in the outer epidermis of the Arabidopsis thaliana sepal. Giant cells undergo endocycles, replicating their DNA without dividing, whereas small cells divide mitotically. We show that distinct enhancers are expressed in giant cells and small cells, indicating that these cell types have different identities as well as different sizes. We find that members of the epidermal specification pathway, DEFECTIVE KERNEL1 (DEK1), MERISTEM LAYER1 (ATML1), Arabidopsis CRINKLY4 (ACR4) and HOMEODOMAIN GLABROUS11 (HDG11), control the identity of giant cells. Giant cell identity is established upstream of cell cycle regulation. Conversely, endoreduplication represses small cell identity. These results show not only that cell type affects cell cycle regulation, but also that changes in the cell cycle can regulate cell type.

1 Follower
  • Source
    • "Apoplastic signalling mediated by ACR4, like DEK1 function, is necessary for the maintenance of HD-ZIP IV gene expression (San-Bento et al., 2014). However, genetic analysis carried out in Arabidopsis and maize (Becraft et al., 2002; Roeder et al., 2012) suggests that DEK1 and ACR4 act in parallel. "
    [Show abstract] [Hide abstract]
    ABSTRACT: During plant epidermal development, many cell types are generated from protodermal cells, a process requiring complex coordination 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.
    Development 05/2015; DOI:10.1242/dev.122325 · 6.27 Impact Factor
  • Source
    • "RESEARCH ARTICLE Development (2015) 142, 1-11 doi:10.1242/dev.117168 DEVELOPMENT (Roeder et al., 2012). The HDG1-mediated increase in cell ploidy in leaves might be a secondary consequence of the increase in margin cells. "
    [Show abstract] [Hide abstract]
    ABSTRACT: AINTEGUMENTA-LIKE (AIL) transcription factors are key regulators of cell proliferation and meristem identity. Although AIL functions have been well described, the direct signalling components of this pathway are largely unknown. We show that BABY BOOM (BBM) and other AIL proteins physically interact with multiple members of the L1-expressed HOMEODOMAIN GLABROUS (HDG) transcription factor family, including HDG1, HDG11 and HDG12. Overexpression of HDG1, HDG11 and HDG12 restricts growth due to root and shoot meristem arrest, which is associated with reduced expression of genes involved in meristem development and cell proliferation pathways, whereas downregulation of multiple HDG genes promotes cell overproliferation. These results suggest a role for HDG proteins in promoting cell differentiation. We also reveal a transcriptional network in which BBM and HDG1 regulate several common target genes, and where BBM/AIL and HDG regulate the expression of each other. Taken together, these results suggest opposite roles for AIL and HDG proteins, with AILs promoting cell proliferation and HDGs stimulating cell differentiation, and that these functions are mediated at both the protein-protein interaction and transcriptional level. © 2015. Published by The Company of Biologists Ltd.
    Development 01/2015; 142(3). DOI:10.1242/dev.117168 · 6.27 Impact Factor
  • BMC Biology 12/2012; 10:101. DOI:10.1186/1741-7007-10-101 · 7.98 Impact Factor
Show more