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The shade avoidance response is mainly evident as increased plant elongation at the expense of leaf and root expansion. Despite the advances in understanding the mechanisms underlying shade-induced hypocotyl elongation, little is known about the responses to simulated shade in organs other than the hypocotyl. In Arabidopsis, there is evidence that shade rapidly and transiently reduces the frequency of cell division in young first and second leaf primordia through a non-cell-autonomous mechanism. However, the effects of canopy shade on leaf development are likely to be complex and need to be further investigated. Using combined methods of genetics, cell biology, and molecular biology, we uncovered an effect of prolonged canopy shade on leaf development. We show that persistent shade determines early exit from proliferation in the first and second leaves of Arabidopsis. Furthermore, we demonstrate that the early exit from proliferation in the first and second leaves under simulated shade depends at least in part on the action of the Homeodomain-leucine zipper II (HD-Zip II) transcription factors ARABIDOPSIS THALIANA HOMEOBOX2 (ATHB2) and ATHB4. Finally, we provide evidence that the ATHB2 and ATHB4 proteins work in concert. Together the data contribute new insights on the mechanisms controlling leaf development under canopy shade.

Shade-intolerant plants perceive the reduction in the ratio of red light (R) to far-red light (FR) as a warning of competition with neighboring vegetation and display a suite of developmental responses known as shade avoidance. In recent years, major progress has been made in understanding the molecular mechanisms underlying shade avoidance. Despite this, little is known about the dynamics of this response and the cascade of molecular events leading to plant adaptation to a low-R/FR environment. By combining genome-wide expression profiling and computational analyses, we show highly significant overlap between shade avoidance and deetiolation transcript profiles in Arabidopsis (Arabidopsis thaliana). The direction of the response was dissimilar at the early stages of shade avoidance and congruent at the late ones. This latter regulation requires LONG HYPOCOTYL IN FAR RED1/SLENDER IN CANOPY SHADE1 and phytochrome A, which function largely independently to negatively control shade avoidance. Gene network analysis highlights a subnetwork containing ELONGATED HYPOCOTYL5 (HY5), a master regulator of deetiolation, in the wild type and not in phytochrome A mutant upon prolonged low R/FR. Network analysis also highlights a direct connection between HY5 and HY5 HOMOLOG (HYH), a gene functionally implicated in the inhibition of hypocotyl elongation and known to be a direct target of the HY5 transcription factor. Kinetics analysis show that the HYH gene is indeed late induced by low R/FR and that its up-regulation depends on the action of HY5, since it does not occur in hy5 mutant. Therefore, we propose that one way plants adapt to a low-R/FR environment is by enhancing HY5 function.

Plants grown under dense canopies perceive through the phytochrome system a reduction in the ratio of red to far-red light as a warning of competition, and this triggers a series of morphological changes to avoid shade. Several phytochrome signaling intermediates acting as positive regulators of accelerated elongation growth and induction of flowering in shade avoidance have been identified. Here we report that a negative regulatory mechanism ensures that in the presence of far-red-rich light an exaggerated plant response does not occur. Strikingly, this unpredicted negative regulatory mechanism is centrally involved in the attenuation of virtually all plant responses to canopy shade.