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. 2017 May 10;18:88. doi: 10.1186/s13059-017-1228-9

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© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 4 — Chromatin remodelers regulate differentiation and proliferation. a In the organizing center of the shoot apical meristem, WUS expression is promoted by chromatin remodeling (via MINU1 and MINU2) and possibly chromatin assembly (involving FAS1). WUS in turn represses differentiation genes such as KANADI1 (KAN) via histone deacetylation (involving TPL and HDA). In the leaf primordium, founder cell driver transcription factors (AS1, AS2, and JLO) repress KNOX gene expression via Polycomb repression, histone deacetylation, and histone variant incorporation (involving PRC2, LHP1, HDA6, and HirA). b In the inflorescence meristem center, stem cell maintenance is promoted by chromatin remodeling (SYD), histone arginine methylation (PRMT5), and a chromatin reader (OBE). SYD directly promotes expression of WUS, a positive regulator of stem cell fate. PRMT5, on the other hand, upregulates CLV3. CLV3 counteracts SAM overproliferation by inhibiting WUS expression. Flower primordium initiation at the flanks of the inflorescence meristem requires an auxin-triggered switch from a compacted chromatin state (TPL/HDA19) to an open chromatin state (BRM/SYD) at MP-bound target genes such as LFY and FIL that promote flower primordium fate. Finally, flower patterning requires the removal of Polycomb repression at floral homeotic genes such as AP3 and AG. This is enabled by the concerted action of the chromatin remodelers SYD and BRM that are recruited by SEP3 and LFY. PKL and histone H3K4 methylation (ATX1, ULT1) also contribute to overcoming Polycomb repression at AP3 and AG. c In different regions of the leaf, the chromatin remodeler BRM promotes either differentiation or cell division. Towards the tip of the leaf, BRM and TCP4 activate the ARR16 TF gene. ARR16 inhibits CK response, which promotes differentiation. At the base of the leaf, BRM and AN3 induce expression of genes encoding the GRF and HEC1 TFs. GRF and HEC1 have been implicated in promoting cell proliferation in the leaf. d After floral organ initiation, the flower meristem terminates. The floral homeotic TF AG represses WUS expression directly and indirectly by promoting Polycomb repression. KNU, a direct target of AG, also represses WUS. The expression of STM, a KNOX gene, is silenced by PRC1. The class A floral homeotic gene AP1 lowers CK hormone levels to promote differentiation. Black, chromatin regulators; blue, transcription factors; green, hormones