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Title: Auxin production in the endosperm drives seed coat development in Arabidopsis }
Article:
Abstract:
In flowering plants, seed development is initiated by the fusion of the maternal egg and central cells with two paternal sperm cells, leading to the formation of embryo and endosperm, respectively. The fertilization products are surrounded by the maternally derived seed coat, whose development prior to fertilization is blocked by epigenetic regulators belonging to the Polycomb Group( PcG) protein family. Here we show that fertilization of the central cell results in the production of auxin and most likely its export to the maternal tissues, which drives seed coat development by removing PcG function. We furthermore show that mutants for the MADS-box transcription factor AGL62 have an impaired transport of auxin from the endosperm to the integuments, which results in seed abortion. We propose that AGL62 regulates auxin transport from the endosperm to the integuments, leading to the removal of the PcG block on seed coat development.
Introduction:
In flowering plants, fertilization of the two female gametes, egg cell and central cell by the two male sperm cells results in the development of the embryo and the endosperm, a nourishing tissue which supports embryo growth. These two fertilization products are surrounded by the seed coat, a sporophytic tissue of purely maternal origin. While the embryo is the only component of the seed that will form the next generation, it contributes little to seed growth. Instead, the interplay between the endosperm and seed coat determines the final size of the seed. Impaired endosperm proliferation has a negative effect on seed coat development, as is the case in the Arabidopsis haiku or miniseed mutants( Garcia et al., 2003; Luo et al., 2005) or in transgenic lines expressing diphtheria toxin A in the endosperm( Weijers et al., 2003). And, conversely, mutations that affect seed coat expansion limit endosperm growth, such as transparent testa glabra 2( Garcia et al., 2005), while mutants with increased integument cell proliferation like megaintegumenta/auxin responsive factor 2, result in enlarged seeds with more abundant endosperm( Schruff et al., 2006). Furthermore, the absence of the endothelium integument layer results in seed abortion, highlighting the importance of the developing seed coat for the establishment of a viable seed( Mizzotti et al., 2012). Endosperm initiation in Arabidopsis is coupled to the production of auxin in the central cell following fertilization( Figueiredo et al., 2015); however, the factor initiating seed coat development is yet to be described. Seed coat initiation is dependent on the fertilization of the female gametophyte, but mutants for sporophytically-acting Polycomb Group( PcG) proteins develop a seed coat without fertilization in a dosage-sensitive manner( Roszak and Köhler, 2011). PcG proteins assemble into multimeric complexes, of which the Polycomb Repressive Complex 2( PRC2) represses target loci through the deposition of trimethyl groups on lysine 27 of histone H3( H3K27me3)( Mozgova et al., 2015). Therefore, the initiation of seed coat development prior to fertilization is inhibited by sporophytically active PRC2 complexes and this block is relieved following fertilization through a signal derived from the fertilization products( Figueiredo and Köhler, 2014; Mozgova et al., 2015). Seed coat development is dependent on the development of the sexual endosperm( Weijers et al., 2003; Ingouff et al., 2006; Roszak and Köhler, 2011), strongly suggesting that the seed coat-initiation signal is generated in the fertilized central cell/endosperm. Here, we show that seed coat development requires production of auxin in the fertilized central cell/endosperm and most likely the transport of auxin to the ovule integuments in an AGL62-dependent manner. We demonstrate that application of auxin is sufficient to drive seed coat development and that AGL62 regulates the expression of P-GLYCOPROTEIN 10( PGP10), in the endosperm, which likely functions as an auxin transporter to the sporophytic tissues. Finally, we show that auxin is sufficient to remove the PRC2 block on seed coat development.
Discussion:
In this manuscript we reveal that auxin is the missing link connecting fertilization and seed coat development. As the maternal integuments do not take part in the fertilization process, the signal that coordinates the development of the fertilization products with the maternal integuments remained elusive( Figueiredo and Köhler, 2016). Based on previous research it seemed likely that the signal is generated in the endosperm, as endosperm development is required to drive seed coat initiation in Arabidopsis( Weijers et al., 2003; Ingouff et al., 2006; Roszak and Köhler, 2011). It was furthermore known that the presence of the paternal genome is necessary for the seed coat to develop, as mutants for cdka;1 and fbl17, in which one of the sperm cells fails to undergo karyogamy with the central cell, do not develop a seed coat( Gusti et al., 2009; Aw et al., 2010). These observations strongly suggest that the signal driving seed coat development should be dependent on genes that are paternally-expressed in the endosperm. Auxin biosynthesis following fertilization of the central cell is dependent on the paternally-expressed genes YUC10 and TAR1( Figueiredo et al., 2015), raising the hypothesis that auxin could be the trigger for seed coat initiation. In this manuscript we provide multiple lines of evidence supporting this hypothesis:( i) auxin rapidly accumulates in the integuments after fertilization,( ii) impaired auxin biosynthesis but not auxin signaling in the endosperm causes defects in seed coat development,( iii) ovules of transgenic lines producing auxin ectopically in the central cell initiate seed coat development without fertilization,( iv) failure of seed coat development in the agl62 mutant correlates with failure to export auxin. Collectively, our data strongly support the hypothesis that auxin generated in the fertilized central cell/endosperm is the trigger for seed coat formation. Impaired auxin signaling in the endosperm did not impair seed coat formation, strongly supporting the hypothesis that auxin is exported to the integuments, where it initiates downstream signaling events. We could show that the ABCB transporter PGP10 is expressed in the fertilized central cell and its expression depends on the type I MADS-box transcription factor AGL62, suggesting that PGP10 may regulate the export of auxin from the endosperm to the integuments. PGPs are known to depend on additional proteins for their localization and function( Bouchard et al., 2006; Wu et al., 2010; Wang et al., 2013), likely explaining our failure to restore seed coat development in agl62 by ectopically expressing PGP10. It is furthermore possible that additional AGL62 targets are required for successful auxin export from the endosperm and are therefore lacking in the agl62 mutant. Future research will focus on identifying the remaining factors required for PGP10 function. Post-fertilization auxin production was shown to lead to activation of GA biosynthesis in the ovules, which is then transported to the valves to promote silique growth( Dorcey et al., 2009). Our observation that auxin produced in the central cell is sufficient to drive parthenocarpic growth of the silique couples the fertilization event to fruit development. We have previously shown that auxin drives endosperm development in Arabidopsis( Figueiredo et al., 2015). We now propose a dual role for post-fertilization auxin production, both in driving endosperm and seed coat development. Additionally, the agl62 mutant has defects both in seed coat development in fertilized ovules and endosperm development in autonomous seeds. This suggests that AGL62, like auxin, is involved in mediating both endosperm and seed coat developmental pathways. It was recently proposed that AGL62 in the endosperm also mediates non-autonomous cell signalling driving nucellus degeneration( Xu et al., 2016). This transcription factor thus seems to be a central player in modulating diverse developmental pathways during seed development. While ectopic auxin production in the central cell was sufficient to initiate seed coat development, the autonomous seeds did not reach the final size of a fertilized seed and collapsed at around 6–7 DAE. This implies that auxin is sufficient to initiate seed coat development, but that additional signals are necessary to support its full expansion and prevent the degeneration of the ovule. Recent work has shown that the innermost layer of the outer ovule integument perceives mechanical cues from the expanding endosperm, which affects cell wall thickening and GA metabolism in that cell layer( Creff et al., 2015). It is therefore an attractive hypothesis that auxin is the initial paternally-derived signal that drives the integument-to-seed coat developmental transition, and that mechanical pressure from the syncytial endosperm sustains seed coat growth. This view is supported by observations showing that mutants affected in syncytial endosperm proliferation have smaller seeds when compared to WT plants( Garcia et al., 2003; Luo et al., 2005; Zhou et al., 2009; Wang et al., 2010). Conversely, a gain-of-function mutation in SHORT HYPOCOTYL UNDER BLUE1 results in increased proliferation of the syncytial endosperm delayed cellularization and increased seed size( Zhou et al., 2009). Additionally, it cannot be ruled out that other signalling pathways contribute to sustain seed coat growth, such as small peptide-mediated signalling( Ingram and Gutierrez-Marcos, 2015; Figueiredo and Köhler, 2016) Mutants in sporophytic PRC2 components develop seed coat autonomously, implying that the PRC2 imposes a block on seed coat development that has to be lifted upon fertilization( Roszak and Köhler, 2011). Here, we demonstrate that ectopic auxin can bypass the PRC2 block on seed coat development, which leads to activation of GA signaling and production of protoanthocyanidins in the integuments. We propose that transport of auxin from the developing endosperm is required for the removal of PRC2 function in the integuments, allowing for the development of the seed coat by activation of GA signaling( Figure 8). Also in mammals PRC2 regulates the transition from proliferation to differentiation during organogenesis and PRC2 function has to be removed to allow differentiation of embryonic stem cells( Leeb et al., 2010; Aldiri and Vetter, 2012). We further show that exogenous auxin is sufficient to remove PRC2 function from the ovule integuments. Our gene expression analysis revealed that sporophytic PRC2-coding genes are downregulated after fertilization, likely due to increased auxin signalling in the integuments. Auxin is known to extensively modulate transcription( Weijers and Wagner, 2016), but the mechanism by which it regulates PRC2-coding genes is yet to be understood. In fact, although there are reports on the transcriptional regulation of PRC2 genes in animals( Neri et al., 2012), there is very little information on how the plant PRC2 activity is regulated. Thus, we provide the first evidence on the modulation of the PRC2 activity by a plant hormone, as a way to modulate developmental transitions. 10. 7554/eLife. 20542. 021Figure 8. Model for the post-fertilization mechanism driving seed coat development. Before fertilization( left panel) sporophytic PRC2 represses seed coat developmental pathways. The fertilization of the central cell( middle panel) results in the production of auxin that is exported to the integuments, lifting the PRC2 block on seed coat development and allowing for cell elongation and differentiation. However, this process is highly dependent on the activity of the transcription factor AGL62, since agl62 seeds fail to export auxin from the endosperm. This leads to auxin accumulation and consequently, failure to develop a seed coat( right panel). We propose that AGL62 activity is important for the expression, and eventually for the activity, of endosperm-specific auxin-exporters. DOI: http://dx. doi. org/10. 7554/eLife. 20542. 021 In conclusion, we have discovered that auxin produced in the fertilized central cell is required to induce seed coat formation after fertilization and most likely acts as mobile signal linking fertilization with the differentiation of the surrounding sporophytic tissues.
The seeds of rice , wheat and other flowering plants store a variety of nutrients , largely in the form of sugars , proteins and oils . These stored reserves provide the main source of calories for humans and livestock all over the world , so they are of major social and economic importance . Seed development is an intricate process . It begins after male sperm cells fuse with female gametes inside the flower . This leads to the formation of the embryo , which will develop into a new plant , and a structure called the endosperm , which nourishes the growing embryo . A protective seed coat surrounds the embryo and endosperm , which develops from certain parts of the parent flower . In order for the seed to develop successfully , these three components have to communicate so they can coordinate their growth . Auxin is a key plant hormone that is needed for plants to grow and develop properly and is necessary for the endosperm to form . Previous research has shown that the endosperm is also required to trigger the formation of the seed coat , but the signal that triggers this process has not yet been identified . Figueiredo et al . now address this question in a small flowering plant called Arabidopsis thaliana . The experiments show that the endosperm produces auxin , which acts as a molecular signal for the seed coat to start forming . Exposing unfertilized flowers to auxin caused a seed coat to form even though the endosperm was absent . This suggests that this hormone alone is sufficient to trigger the formation of the seed coat without any other signals . Further analysis revealed that a protein called AGL62 regulates the movement of auxin to the parts of the flower that give rise to the seed coat . In the absence of AGL62 , the hormone remains trapped in the endosperm and the seed coat fails to develop . The next step following on from this work is to understand how auxin moves from the endosperm to the parts of the flower that form the seed coat .