Preliminary Characterization Of PHYA-mediated Shade Tolerance Response In Strong Shade

Plants have developed two growth strategies when shade adverse environment was perceived,they are shade avoidance and shade tolerance.Shade avoidance displays a series of typical shade syndrome,including elongation of stem and petiole,lower chlorophyll content,while shade tolerance has an increased specific leaf area(SLA)and decreased chlorophyll a/b ratio.Compared to the relatively well-developed study system for shade avoidance,the molecular mechanism of shade tolerance has been understood poorly.In our strong shade(R:FR=0.1)condition,the wild type Col-0 has no elongated hypocotyl as shade condition(R:FR=0.1),but similar to which in white light.And higher chlorophyll content was observed in strong shade compared to shade.Interestingly,the mutant phyA-211 has longer hypocotyl and lower chlorophyll content than Col-0 in strong shade.We consider that shade-avoided plant Arabidopsis thaliana go into shade tolerance period under continuous strong shade condition,and PHYA involved in this process.We found that PIF4/PIF5 partially involved in the PHYA-mediated shade tolerance in strong shade,while COP1 completely involved in it.Besides,our microarray data showed that 506 genes were down-regulated in phyA-211 mutant under strong shade treatment for 24 hours compared to Col-0,which also down-regulated by ABA,sucrose or hypoxia treatment in Genevestigator.In our data,we found that sucrose treatment eliminated the shade tolerance phenotypes in strong shade,which revealed that continuous strong shade brings plant into an energy starvation status.Corresponding to the energy shortage,SnRK1 pathway,the important growth inhibition pathway in plant,was dramaticlly activated in strong shade,and PHYA inhibit its activation.We also found that PHYA probably inhibit ABA signaling in shade and strong shade.Furthermore,we observed an equally distinct activation of ERF72 in shade and strong shade 24 hours,which had partial decrease in ein3-1 mutant,cch mutant and completely defect in ein2-5 mutant.