Further Development 3.4: Polycomb and Trithorax Proteins Regulate the Leaf-to-Flower Transition in Plants

Differential Gene Expression: Mechanisms of Cell Differentiation

Hyacinths bloom in the spring, lilies often reveal their petals during the summer months, and dahlia flowers persist well into autumn. Aside from the glorious colors and sensational scents of flowers, their presence marks the transition of a plant from its vegetative to its reproductive state. This transition requires a change in the cell types and organs produced by the shoot apical meristem (SAM) (Figure 1A). During the vegetative state, the SAM primarily generates leaves; however, when the time is right for reproduction, this stem cell factory builds flowers. Depending on the species, this most often involves producing sepals, petals, stamens, and carpels. Developing its reproductive parts at the wrong time could be catastrophic for the plant’s survival. The temperature, amount of sunlight, and availability of nutrients must all be conducive to reproductive growth. Of equal importance is synchronizing the plant’s gamete production with the presence of potential pollinators (Figure 1B). Therefore, the initiation of the SAM transition to a reproductive state is a critical regulatory event during plant development (see Chapter 6). The genetic control of this process is at least in part epigenetic, involving proteins homologous to Polycomb and Trithorax proteins.

How epigenetics “opens” the flower

Just as environmental cues influence the initiation of flower development, epigenetic factors control the developmental conversion of the SAM from leaf to flower construction. This can be tested experimentally simply by moving a plant to long-day conditions and observing the upregulation of floral gene activity in the SAM (Figure 1C; You et al. 2017a). During vegetative growth, the genes that promote reproductive organogenesis are actively silenced. When environmental conditions are optimal for reproductive success, the repression of these genes is removed. The entire developmental program for flowering is regulated through epigenetic mechanisms mediated by a set of chromatin-modifying proteins that are deeply homologous to the Polycomb and Trithorax groups. Although exceptions are being discovered, Polycomb Repressive Complexes 1 and 2 (PRC1 and PRC2) bind to specific regions of the chromatin to inactivate those regions as well as maintain their repressed state (Figure 1D). Specifically, PRC1 proteins repress transcription and/or condense the chromatin through histone ubiquitylation, and PRC2 proteins use histone methylation to further maintain these repressive states. In contrast, Trithorax proteins reverse these repressed states and promote activation of the floral MADS-box genes (plant transcription factors that determine the identity of floral parts). Loss of the Polycomb genes causes the upregulation of these floral organ identity genes and precocious flower development (reviewed in Merini and Calonje 2015; Pu and Sung 2015).

Figure 1Polycomb and Trithorax proteins are epigenetic regulators of the leaf-to-flower transition. (A) Environmental cues trigger the shoot apical meristem (SAM) to transition from vegetative growth (leaves) to reproductive growth (flowers) capable of producing all the floral organs (right). (B) Timing of this transition is critical for the coordination of many factors, one being the presence of pollinators, such as the bee shown here. (C) Floral MADS-box gene expression is upregulated in the SAM following exposure to long-day conditions. Expression of the MADS-box gene APETALA1 (AP1) is shown here. (D) Generalized model of Polycomb repressive and Trithorax activating complexes of MADS-box floral gene expression. Polycomb Repressive Complex 1 (PRC1) proteins repress transcription and/or compact chromatin through histone ubiquitylation (green circle), and PRC2 proteins use histone methylation (red) to further maintain these repressive states. In contrast, Trithorax proteins antagonize repressed states and promote activation of the floral MADS-box genes. (D after W. Merini and M. Calonje. 2015. Plant J 83: 110–120.)

Developing Questions

From the greater environment to the cellular environment, how are epigenetic states regulated by external environmental signals?

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