The AGL62 MADS Domain Protein Regulates Cellularization during Endosperm Development inArabidopsis 

Abstract

Endosperm, a storage tissue in the angiosperm seed, provides nutrients to the embryo during seed development and/or to the developing seedling during germination. A major event in endosperm development is the transition between the syncytial phase, during which the endosperm nuclei undergo many rounds of mitosis without cytokinesis, and the cellularized phase, during which cell walls form around the endosperm nuclei. The molecular processes controlling this phase transition are not understood. In agl62 seeds, the endosperm cellularizes prematurely, indicating that AGL62 is required for suppression of cellularization during the syncytial phase. AGL62 encodes a Type I MADS domain protein that likely functions as a transcription factor. During seed development, AGL62 is expressed exclusively in the endosperm. During wild-type endosperm development, AGL62 expression is strong during the syncytial phase and then declines abruptly just before cellularization. By contrast, in mutant seeds containing defects in some FERTILIZATION-INDEPENDENT SEED (FIS) class Polycomb group genes, the endosperm fails to cellularize and AGL62 expression fails to decline. Together, these data suggest that AGL62 suppresses cellularization during the syncytial phase of endosperm development and that endosperm cellularization is triggered via direct or indirect AGL62 inactivation by the FIS polycomb complex.

The Differential Transcription Network between Embryo and Endosperm in the Early Developing Maize Seed

“…S17), implicating a differential transcriptional regulation between embryo and endosperm. It was previously reported that TFs of MADS function in seed and endosperm development (Kang et al, 2008;Sreenivasulu et al, 2008;Bemer et al, 2010;Le et al, 2010;Agarwal et al, 2011;Hehenberger et al, 2012). AGL62, a MADS protein of Arabidopsis, is the direct target of FIS Polycomb group repressive complex2 (PRC2), establishing the molecular basis for FIS PRC2-mediated endosperm cellularization (Hehenberger et al, 2012).…”

Mechanisms and evolution of genomic imprinting in plants

“…Developmental defects are associated with increased expression of PHE1 and many other genes in the endosperm (Kang et al, 2008;Kö hler et al, 2003b;Erilova et al, 2009), suggesting that the main function of the FIS PcG complex is to suppress dosage sensitive genes in the endosperm. Support for this idea stems from experiments showing that fis mutants can form viable seeds if a sexually derived fis embryo is supported by an autonomously developing diploid endosperm (Nowack et al, 2007).…”

Networks controlling seed size in Arabidopsis

“…The existence of three redundant pathways that 144 control endosperm cellularization has been recently pro-145 posed (Kang et al 2013). The first pathway regulates 146 endosperm cellularization through the action of APETALA 147 2 (AP2) and the MADS-box transcription factor AGL62 148 (Kang et al 2008 (Jofuku et al 1994;Okamuro et al 1997;Riechmann and 159 Meyerowitz 1998). AP2 is involved in a great variety of 160 developmental processes, including endosperm cellular-161 ization.…”

“…The expression 171 level AGL62 correlates with endosperm cellularization in a 172 dosage-dependent way, suggesting that it represents a key 173 regulator of endosperm cellularization and consequently of 174 seed size determination. Accordingly, the agl62 mutants 175 have precocious endosperm cellularization and a small 176 seed phenotype (Kang et al 2008;Kradolfer et al 2013), 177 while increased AGL62 expression correlates with a delay …”

“…2). 301 Finally, it is necessary to mention that perturbation of 302 the relative dosages of the maternal and paternal genomes, 303 typical in the case of interploidy crosses, directly affects 304 endosperm development and seed size (Garcia et al 2003;305 Luo et al 2005;Kang et al 2008;Zhou et al 2009;Wang 306 et al 2010). The defects and low endosperm viability often 307 observed in seeds of interploidy crosses (as in the case of 308 wheat) can be explained in terms of maternal or paternal 309 genome excess, i.e., an imbalance between MEGs and 310 PEGs, and its effect on endosperm growth (Haig and 311 Westoby 1991).…”