One fascinating observation is the coordination that is often observed between the responses of different organs. This can lead to unexpected outcomes in one aspect of photomorphogenesis when a separate aspect is altered. Specifically, signals that suppress the elongation of the etiolated hypocotyl often also cause the unfolding of cotyledons, a degree of leaf development and even expression of photosynthetic genes. For example, the loss of brassinosteroids, hormones which also primarily affect cell expansion responses, in Arabidopsis det2 causes a short hypocotyl and unfolded cotyledons in the dark, but is also accompanied by a degree of leaf development, including the expression of photosynthesis-related genes (Li et al. 1996). The same is true following the chemical or genetic suppression of GA production in pea and Arabidopsis (Alabadi et al. 2004), and, to some extent, also following the inhibition of auxin signalling through SHY2 (Tian et al. 2002). A direct screen for mutants, which showed de-repression of photosynthesis-related genes in the dark, yielded the Dark overexpressor of Cab 1 (doc1) mutant. The doc1 mutation, showing minimal morphological phenotypes at the seedling stage, in darkness or light, nevertheless turned out to be caused by a defect in the BIG gene, encoding a callosin-like protein with a role in auxin transport (Gil et al. 2001). Again this indicates a link between a hormone involved in the control of (hypocotyl) organ growth and a response that is part of the differentiation programme of cotyledon photosynthetic cells. The nature of this link is one of the most central, standing questions in the understanding of the control of growth responses by light.
At present it is only possible to speculate about the link above. However, it may be useful to conceptualise the phenomenon as part of the fundamental decision that takes place near meristems, a decision between cellular proliferation (and possibly expansion) on the one hand, and differentiation of mature cells on the other. Cell cycle progression is ultimately driven by genes under the control of transcription factors of the E2F family. E2Fs are post-translationally regulated by the repressive binding of the retinoblastoma-related (RBR1) protein, with the activity of RBR1 being, in turn, controlled by phosphorylation by cyclin-dependent kinases, the primary cell cycle regulators (De Veylder et al. 2007). From deregulated expression studies a picture is gradually emerging in which different E2F factors can have different, even opposite, functions, with E2FA being associated with entry into DNA synthesis (S) phase and E2FB being associated with S phase and with entry into mitosis, while E2FC represses cell cycle activity and initiates differentiation responses (De Veylder et al. 2007). In fact these transcription factors could, themselves, be direct targets of light signalling pathways. For example, expression of E2FC can be observed in dark-grown hypocotyls, and is destabilised in the light (del Pozo et al. 2002). We have directly observed the control of E2FC and E2FB protein levels by light and by photomorphogenesis regulators, COP1, DET1 and CSN subunit 5 (Magyar, Lopez-Juez and Bogre, unpublished observations). This is not completely surprising, given the fact that de-etiolation involves the removal of the repression of the normal growth programme, and that the ancestral function of COP1 and the CSN in other organisms is related to the control of cell cycle and differentiation (Doronkin et al. 2003; Wei and Deng 2003). It is also worth noting that the ectopic expression of RBR in shoot meristems has been shown to result in cellular vacuolation, a phenomenon normally associated with differentiation, and with the increased expression of photosynthesis-related genes (Wyrzykowska et al. 2006). Therefore, photomorphogenic regulators could be at the heart of the decisions involving basic cell growth and differentiation in the proximity of the meristem.
Regulation of cell proliferation or differentiation through RBR1 and E2Fs adds another layer, possibly a basal one, to our understanding of photomor-phogenesis. RB, specifically, affects gene regulation by recruiting chromatin remodelling enzymes in animal cells (Du and Pogoriler 2006). Although it is at present unclear whether this is related to RB-dependent gene regulation, it is known that modification of chromatin plays a role in de-etiolation growth responses. For example, DET1 is capable of association with histones and of causing their post-translational modification (Benvenuto et al. 2002), while loss of HAF2, a transcription cofactor, causes reduced acetylation of histone H3 in light-responsive promoters and reduced ability to de-etiolate (Bertrand et al. 2005). Clearly unravelling the growth/differentiation link will be an important milestone in our understanding of the control of growth and of its response to light in plants.
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