公开(公告)号：US07164013B2

公开(公告)日：2007-01-16

申请号：US10641100

申请日：2003-08-15

申请人： Moon-Soo Soh ,  Pill-Soon Song ,  Ki-Young Yang

发明人： Moon-Soo Soh ,  Pill-Soon Song ,  Ki-Young Yang

IPC分类号： C12N15/29 ,  C12N15/52

CPC分类号： C12N15/8237

摘要： This invention is about the functionally hyperactive light signal related molecule, HFR1-ΔN105, 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-ΔN105 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-ΔN105 overexpressing plants. These results suggest that N-terminal region of HFR1 negatively regulate HFR1 function and that HFR1-ΔN105 is hyperactive.

摘要翻译： 本发明涉及功能性超活动光信号相关分子HFR1-DeltaN105，其中编码N末端105个氨基酸残基的核酸被缺失。 HFR1作为bHLH转录因子在植物色素A信号级联的一个子集中起作用，据报道COP1负调节。 HFR1-DeltaN105过表达植物的实验显示，N末端氨基酸的缺失使得HFR1在光形态发生如萌发和脱乙酰化中更具活性。 此外，转基因植物在抑制下胚轴延伸方面表现出过敏光响应，依赖于光信号传导的另一阳性元件bZIP蛋白HY5。 在HFR1-DeltaN105过表达植物中，终末的远红光反应和叶柄伸长被抑制。 这些结果表明，HFR1的N末端区域负调节HFR1功能，HFR1-DeltaN105是多活性的。

公开(公告)号：US20050039225A1

公开(公告)日：2005-02-17

申请号：US10641100

申请日：2003-08-15

申请人： Moon-Soo Soh ,  Pill-Soon Song ,  Ki-Young Yang

发明人： Moon-Soo Soh ,  Pill-Soon Song ,  Ki-Young Yang

IPC分类号： C12N15/82 ,  A01H1/00 ,  C07H21/04 ,  C12N5/04 ,  C12N9/02

CPC分类号： C12N15/8237

摘要： This invention is about the functionally hyperactive light signal related molecule, HFR1-ΔN105, 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-ΔN105 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-ΔN105 overexpressing plants. These results suggest that N-terminal region of HFR1 negatively regulate HFR1 function and that HFR1-ΔN105 is hyperactive.

摘要翻译： 本发明涉及功能性超活动光信号相关分子HFR1-DeltaN105，其中编码N末端105个氨基酸残基的核酸被缺失。 HFR1作为bHLH转录因子在植物色素A信号级联的一个子集中起作用，据报道COP1负调节。 HFR1-DeltaN105过表达植物的实验显示，N末端氨基酸的缺失使得HFR1在光形态发生如萌发和脱乙酰化中更具活性。 此外，转基因植物在抑制下胚轴延伸方面表现出过敏光响应，依赖于光信号传导的另一阳性元件bZIP蛋白HY5。 在HFR1-DeltaN105过表达植物中，终末的远红光反应和叶柄伸长被抑制。 这些结果表明，HFR1的N末端区域负调节HFR1功能，HFR1-DeltaN105是多活性的。