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Signaling from the embryo conditions Vp1‐mediated repression of α‐amylase genes in the aleurone of developing maize seeds
Author(s) -
Hoecker Ute,
Vasil Indra K.,
McCarty Donald R.
Publication year - 1999
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.1999.00521.x
Subject(s) - aleurone , embryo , psychological repression , amylase , gene , biology , endosperm , microbiology and biotechnology , botany , genetics , enzyme , gene expression , biochemistry
Summary The VP1 transcription factor functions as both a repressor and an activator of gene expression in the developing aleurone. Vp1 activation of the anthocyanin pathway exhibits strict cell autonomy in aleurone. In contrast, Vp1‐mediated repression of hydrolase genes in aleurone cells during seed development is determined by a combination of cell autonomous and cell non‐autonomous signals. To analyze signaling between the embryo and aleurone during seed development, a T‐B3La chromosome translocation was used to create seed that has non‐concordant embryo and endosperm genotypes. We show that de‐repression of an Amy‐GUS reporter gene in developing vp1 mutant aleurone cells strongly depends on the presence of a viviparous embryo. Genetic ablation of the developing embryo in vp1 mutant and Vp1 seeds through the introduction of an early embryo mutation caused a similar enhancement of Amy‐GUS expression in the aleurone, suggesting that the quiescent embryo present in normal seed is a critical source of inhibitory signals. Analysis of an ABA deficient vp1 vp5 double mutant indicates that ABA synthesized in the embyro interacts additively with Vp1 to prevent precocious induction of α‐amylase genes in the aleurone of the developing seed. A lack of ABA synthesis, however, does not account for the strongly synergistic interaction between a viviparous vp1 embryo and mutant aleurone suggesting that a quiescent embyro is a source of other inhibitory signals.

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