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Complex structure of a maize Myb gene promoter: functional analysis in transgenic plants
Author(s) -
Sidorenko Lyudmila V.,
Li Xianggan,
Cocciolone Suzy M.,
Chopra Surinder,
Tagliani Laura,
Bowen Ben,
Daniels Michael,
Peterson Thomas
Publication year - 2000
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1046/j.1365-313x.2000.00750.x
Subject(s) - biology , enhancer , gene , genetics , promoter , transgene , reporter gene , regulatory sequence , myb , transcription factor , transcription (linguistics) , gene expression , microbiology and biotechnology , linguistics , philosophy
Summary The maize P gene encodes a Myb‐like transcription factor that regulates synthesis of red flavonoid pigments in floral organs. To study the transcriptional regulation of the P gene, candidate regulatory sequences of the P1‐rr gene promoter were identified by Ac insertional mutagenesis and subjected to functional testing in transgenic maize plants. The results indicate that a 561 bp fragment (Pb) encompassing the transcription start site (−235 to +326) supports weak expression of a GUS reporter gene in floral organs, including husk, silk, kernel pericarp, cob and male inflorescence. Two other fragments, located approximately 1 and 5 kb 5′ of the transcription start site, increased the levels of GUS activity in floral tissues and thus appear to contain enhancer elements. All of the tested constructs gave similar patterns of GUS expression, suggesting that the 561 bp Pb fragment that is common among the transgene constructs contains regulatory elements that promote activation in floral organs. The basal promoter and proximal enhancer fragments contain putative binding sites for bZip regulatory factors, and a complex arrangement of palindromes including a large inverted repeat of two tRNA‐like genes. Possibly, interconversions between linear and cruciform conformations of the palindromes may affect protein/DNA interactions and thereby modulate P1‐rr expression.