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Spatiotemporal Restriction of FUSCA3 Expression by Class I BPCs Promotes Ovule Development and Coordinates Embryo and Endosperm Growth.
The Plant Cell ( IF 11.6 ) Pub Date : 2020-06-01 , DOI: 10.1105/tpc.19.00764
Jian Wu 1, 2 , Deka Mohamed 2, 3 , Sebastian Dowhanik 2 , Rosanna Petrella 4 , Veronica Gregis 4 , Jingru Li 1 , Lin Wu 2, 5 , Sonia Gazzarrini 3, 6
Affiliation  

Spatiotemporal regulation of gene expression is critical for proper developmental timing in plants and animals. The transcription factor FUSCA3 (FUS3) regulates developmental phase transitions by acting as a link between hormonal pathways in Arabidopsis (Arabidopsis thaliana). However, the mechanisms governing its spatiotemporal expression pattern are poorly understood. Here, we show that FUS3 is repressed in the ovule integuments and seed endosperm. FUS3 repression requires class I BASIC PENTACYSTEINE (BPC) proteins, which directly bind GA/CT cis-elements in FUS3 and restrict its expression pattern. During vegetative and reproductive development, FUS3 derepression in bpc1-1 bpc2 (bpc1/2) double mutant or misexpression in ProML1:FUS3 lines causes dwarf plants carrying defective flowers and aborted ovules. After fertilization, ectopic FUS3 expression in bpc1/2 endosperm or ProML1:FUS3 endosperm and endothelium increases endosperm nuclei proliferation and seed size, causing delayed or arrested embryo development. These phenotypes are rescued in bpc1/2 fus3-3. Finally, class I BPCs interact with FIS-PRC2 (FERTILIZATION-INDEPENDENT SEED-Polycomb Repressive Complex2), which represses FUS3 in the endosperm during early seed development. We propose that BPC1 and 2 promote the transition from reproductive to seed development by repressing FUS3 in ovule integuments. After fertilization, BPC1 and 2 and FIS-PRC2 repress FUS3 in the endosperm to coordinate early endosperm and embryo growth.



中文翻译:

I类BPC对FUSCA3表达的时空限制会促进胚珠发育并协调胚胎和胚乳的生长。

基因表达的时空调节对于植物和动物的适当发育时机至关重要。转录因子FUSCA3(FUS3)通过充当拟南芥(Arabidopsis thaliana)激素途径之间的链接来调节发育相变。但是,对其时空表达模式进行控制的机制了解甚少。在这里,我们显示FUS3被抑制在胚珠外皮和种子胚乳中。FUS3压制需要I类BASIC PENTACYSTEINE(BPC)的蛋白质,它直接结合GA / CT CIS在-elements FUS3和限制其表达模式。在营养和生殖发育过程中,FUS3去阻遏在bpc1-1 bpc2bpc1 / 2)在双突变体或错误表达ProML1:FUS3线使得实施有缺陷的鲜花和中止胚珠矮化植株。受精后,异位FUS3bpc1 / 2胚乳或ProML1:FUS3胚乳和内皮中的表达增加胚乳细胞核的增殖和种子大小,导致胚胎发育延迟或停止。这些表型在bpc1 / 2 fus3-3得以拯救。最后,I类BPC与FIS-PRC2(不依赖肥料的SEED-Polycomb阻抑复合物2)相互作用,从而抑制FUS3种子发育早期在胚乳中。我们建议BPC1和2通过抑制胚珠外皮中的FUS3促进从生殖到种子发育的过渡。受精后,BPC1和2和FIS-PRC2抑制胚乳中的FUS3,以协调早期胚乳和胚的生长。

更新日期:2020-06-01
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