Dear Editor,rnPlants grown in close proximity experience a change in light quality,and respond by reallocating energy resources from storage organs to stem-like organs.This adaptive response,called the shade-avoidance syndrome (SAS),allows the shaded plant to grow and compete effectively against its neighbors.SAS is initiated upon detection by the phytochrome photoreceptors of a lowering of the ratio of red to far-red light (R/FR),leading to the synthesis of plant hormones and a transcriptional cascade that targets genes involved in growth.Among these genes is PIL1 (PHYTOCHROME INTERACTING FACTOR 3-LIKE 1),which encodes a bHLH transcription factor,whose expression is induced by up to 100-fold within 30min of exposure to shade (Salter et al.,2003);yet,PIL1’s precise role in shade avoidance is unknown.The Salter paper concluded that PIL1 worked with TOC1 to restrict growth to a particular time of day,and that PIL1 is necessary for the normal display of the rapid elongation response to shade (Salter et al.,2003).Later,Roig-Villanova and colleagues (2006) showed that PIL1 is a negative regulator of the SAS with only phenotype of pil1-4 and pil1-4phyB without any mechanism.To further understand the function of PIL1 in transducing phytochrome signals during the shade-avoidance response,we examined phenotypes of PIL1 loss-and gain-of-function mutants in simulated shade and proposed three possible modes of PIL1 action based on its protein stability and interaction with DNA and PIFs to regulate gene expression.