This invention is about the functionally hyperactive light signal related molecule, HFR1-.DELTA.N105, of which the nucleic acids that encode N-terminal 105 amino acid residues were deleted. HFR1 as a bHLH transcription factor functions in a subset of phytochrome A signaling cascade and it was reported to be regulated negatively by COP1. Experiments with a HFR1-.DELTA.N105 overexpressing plant revealed that the deletion of N-terminal amino acids makes the HFR1 more active in photomorphogenic development such as germination and de-etiolation. In addition, the transgenic plants showed hypersensitive photo-responses in the inhibition of hypocotyl elongation, dependently on another positive element of light signaling, a bZIP protein, HY5. The end-of-day far-red light response and petiole elongation were suppressed in the HFR1-.DELTA.N105 overexpressing plants. These results suggest that N-terminal region of HFR1 negatively regulate HFR1 function and that HFR1-.DELTA.N105 is hyperactive.