Transcriptional Regulation in Plants


Transcriptional regulation encompasses all of the events leading up to a change in gene expression status, either activation or repression. Although many of the mechanisms of transcriptional regulation are shared between plants and animals, plants are distinctly different in that they rely more heavily on subtle environmental cues than animals do because they are sessile, and they continue to develop new organs post‐embryonically. These unusual features require constant refinement at the transcriptional level to implement large‐scale gene expression changes. Many signalling pathways converge at the level of transcription in plants, including hormone‐response pathways and light‐response pathways, forming complex gene regulatory networks and intricate feed‐back loops to control the growth and development of plants. Additionally, alterations to the chromatin such as deoxyribonucleic acid (DNA) methylation and histone modifications can also affect transcriptional regulation and even lead to the formation of epialleles and genomic imprinting.

Key Concepts:

  • Transcriptional regulation in plants relies on many of the same mechanisms as transcriptional regulation in animals but with subtle variations.

  • Plant hormones, such as auxin, play a major instructive role in gene expression.

  • Because plants are sessile organisms, environmental cues (e.g. quality and quantity of light) are critical for regulating transcription and affect the timing of developmental decisions.

  • DNA and histone methylation can alter gene expression and contributes to the formation of heritable epialleles and imprinting.

Keywords: Transcriptional regulation; gene regulatory networks; epigenetics; feed‐back loop; Arabidopsis

Figure 1.

Life cycle of Arabidopsis, from embryogenesis to the next generation. (a) Heart‐stage embryo. Green shading indicates developing shoot tissue, blue shading marks root apical meristem. (b) Seedling stage. (c) Adult stage. (d) Developing embryo within the seed (adapted from

Figure 2.

Auxin gradients instruct apical/basal patterning during embryogenesis. (a) Auxin (pink) flow and maxima are established in the embryo by the PIN efflux proteins. These levels are interpreted by the plant at the level of transcription. (b) Hypothetical model for PLETHORA (PLT1/2) gene activation. PLT1/2, master regulators of root fate, are activated in the root apical meristem (RAM), where auxin levels are high, in an auxin response factor (ARF)‐dependent manner, although direct binding of ARF to the promoter has not been reported. Auxin binds to TIR1, which in turn binds to the ARF binding partner, IAA, and targets IAA for degradation via the 26S proteasome. In the shoot apical meristem (SAM), an area of low auxin concentration, PLT1/2 are repressed through the concerted action of an IAA transcription factor that binds to and prevents the ARF from activating transcription as well as recruits the corepressor TPL.

Figure 3.

The shoot apical meristem (SAM) is a stem cell niche regulated by a transcriptional feed‐back circuit that spatially controls CLAVATA1 (CLV1), CLAVATA2 (CLV2) and WUSCHEL (WUS). WUS specifies stem cell fate in the organising centre of the L3 layer. It is repressed in part through the action of CLV1, a leucine‐rich receptor kinase expressed in the L1 and L2 layers but migrates to the L3 layer that binds to the mobile glycopeptide CLV3. Through an indirect mechanism, WUS activates CLV3, leading to a feed‐back loop. Additionally, WUS binds to and represses CLV1. Figure partially adapted from Clark .

Figure 4.

Light regulation of CONSTANS (CO), a key regulator of flowering time. Under long day conditions, CO is activated by GIGANTEA (GI) and FLAVIN‐BINDING, KELCH REPEAT, F‐BOX 1 (FKF1), which negatively regulate CYCLING DOF FACTOR1 (CDF1). Under short day conditions, CDF1 can bind to and repress CO.CO is also regulated post‐transcriptionally by light. In the absence of light, the E3 ligase COP1 targets CO for degradation. In the presence of light, the cryptochrome CRY2 interacts with COP1, releasing CO, which then activates FLOWERING LOCUS T (FT). FT is transported from the leaf to the shoot apical meristem where it interacts with FLOWERING LOCUS D (FD). Together, FT and FD activate genes promoting flowering, including the floral identity gene APETALA1 (AP1).

Figure 5.

Maternal and paternal genomes make different contributions to the developing embryo. In the endosperm, MEDEA (MEA) is expressed only from the maternal genome, and it is activated by DEMETER (DME), which maintains the chromatin in an open, hypomethylated state. MEA acts as part of a complex that deposits H3K27 dimethylation at the paternal MEA and maternal PHERES1 (PHE) loci.



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Further Reading

Chapman EJ and Estelle M (2009) Mechanism of auxin‐regulated gene expression in plants. Annual Review of Genetics 43: 265–285.

Moazed D (2011) Mechanisms for the inheritance of chromatin states. Cell 146: 510–518.

Srikanth A and Schmid M (2011) Regulation of flowering time: all roads lead to Rome. Cellular and Molecular Life Sciences 68: 2013–2037.

Vanneste S and Friml J (2009) Auxin: a trigger for change in plant development. Cell 136: 1005–1016.

Zhang X (2008) The epigenetic landscape of plants. Science 320: 489–492.

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Macrae, Rhiannon K, and Long, Jeffrey A(May 2012) Transcriptional Regulation in Plants. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1002/9780470015902.a0023755]