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LATE, a C 2 H 2 zinc‐finger protein that acts as floral repressor
Author(s) -
Weingartner Magdalena,
Subert Christa,
Sauer Norbert
Publication year - 2011
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 - 10.1111/j.1365-313x.2011.04717.x
Subject(s) - meristem , biology , primordium , ectopic expression , arabidopsis , repressor , botany , transcription factor , zinc finger , phloem , microbiology and biotechnology , vernalization , apical dominance , gene , arabidopsis thaliana , photoperiodism , genetics , shoot , mutant
Summary The transition from vegetative to generative development is a major developmental switch in flowering plants and is critical for reproductive success. This transition requires reprogramming of lateral primordia at the shoot apical meristem, which leads to the formation of determinate floral meristems instead of leaves. In Arabidopsis, flowering is induced by a network of interacting pathways. In the photoperiod‐dependent pathway, the two key elements mediating the effect of day length on flowering time are the transcription factors CONSTANS (CO) and the phloem mobile flowering signal FLOWERING LOCUS T (FT). Here, we identify a factor that is critically involved in this flowering response. The gene, which we named LATE FLOWERING ( LATE ), encodes a C 2 H 2 ‐type zinc‐finger transcriptional regulator, and is expressed in the leaf vasculature and the vegetative shoot apical meristem. Ectopic expression of LATE in all tissues results in a dose‐dependent phenotype characterized by late flowering, altered floral organ identity and sterile flowers. Using tissue‐specific promoters, we further show that LATE controls the transition to flowering at two levels: first, it regulates the expression of flowering time genes in the leaf vasculature, and second, it interferes with floral meristem identity genes at the apex.