Transcriptional Regulation of Arabidopsis Polycomb Repressive Complex 2 Coordinates Cell Type Proliferation and Differentiation

Spatiotemporal regulation of transcription is fine-tuned at multiple levels, including chromatin compaction. Polycomb Repressive Complex 2 (PRC2) catalyzes the trimethylation of Histone 3 at lysine 27 (H3K27me3), which is the hallmark of a repressive chromatin state. Multiple PRC2 complexes have been reported in Arabidopsis thaliana to control the expression of genes involved in developmental transitions and maintenance of organ identity. Here, we show that PRC2 member genes display complex spatiotemporal gene expression patterns and function in root meristem and vascular cell proliferation and specification. Furthermore, PRC2 gene expression patterns correspond with vascular and non-vascular tissue-specific H3K27me3-marked genes. This tissue-specific repression via H3K27me3 regulates the balance between cell proliferation and differentiation. Using enhanced yeast-one-hybrid analysis, upstream regulators of the PRC2 member genes are identified, and genetic analysis demonstrates that transcriptional regulation of some PRC2 genes plays an important role in determining PRC2 spatiotemporal activity within a developing organ

Polycomb Repressive Complex 2 Controls the Embryo-to-Seedling Phase Transition

Polycomb repressive complex 2 (PRC2) is a key regulator of epigenetic states catalyzing histone H3 lysine 27 trimethylation (H3K27me3), a repressive chromatin mark. PRC2 composition is conserved from humans to plants, but the function of PRC2 during the early stage of plant life is unclear beyond the fact that it is required for the development of endosperm, a nutritive tissue that supports embryo growth. Circumventing the requirement of PRC2 in endosperm allowed us to generate viable homozygous null mutants for FERTILIZATION INDEPENDENT ENDOSPERM (FIE), which is the single Arabidopsis homolog of Extra Sex Combs, an indispensable component of Drosophila and mammalian PRC2. Here we show that H3K27me3 deposition is abolished genome-wide in fie mutants demonstrating the essential function of PRC2 in placing this mark in plants as in animals. In contrast to animals, we find that PRC2 function is not required for initial body plan formation in Arabidopsis. Rather, our results show that fie mutant seeds exhibit enhanced dormancy and germination defects, indicating a deficiency in terminating the embryonic phase. After germination, fie mutant seedlings switch to generative development that is not sustained, giving rise to neoplastic, callus-like structures. Further genome-wide studies showed that only a fraction of PRC2 targets are transcriptionally activated in fie seedlings and that this activation is accompanied in only a few cases with deposition of H3K4me3, a mark associated with gene activity and considered to act antagonistically to H3K27me3. Up-regulated PRC2 target genes were found to act at different hierarchical levels from transcriptional master regulators to a wide range of downstream targets. Collectively, our findings demonstrate that PRC2-mediated regulation represents a robust system controlling developmental phase transitions, not only from vegetative phase to flowering but also especially from embryonic phase to the seedling stage

A network of transcriptional repressors modulates auxin responses.

International audienceThe regulation of signalling capacity, combined with the spatiotemporal distribution of developmental signals themselves, is pivotal in setting developmental responses in both plants and animals1. The hormone auxin is a key signal for plant growth and development that acts through the AUXIN RESPONSE FACTOR (ARF) transcription factors2-4. A subset of these, the conserved class A ARFs5, are transcriptional activators of auxin-responsive target genes that are essential for regulating auxin signalling throughout the plant lifecycle2,3. Although class A ARFs have tissue-specific expression patterns, how their expression is regulated is unknown. Here we show, by investigating chromatin modifications and accessibility, that loci encoding these proteins are constitutively open for transcription. Through yeast one-hybrid screening, we identify the transcriptional regulators of the genes encoding class A ARFs from Arabidopsis thaliana and demonstrate that each gene is controlled by specific sets of transcriptional regulators. Transient transformation assays and expression analyses in mutants reveal that, in planta, the majority of these regulators repress the transcription of genes encoding class A ARFs. These observations support a scenario in which the default configuration of open chromatin enables a network of transcriptional repressors to regulate expression levels of class A ARF proteins and modulate auxin signalling output throughout development

Apple russeting as seen through the RNA-seq lens: strong alterations in the exocarp cell wall

Russeting, a commercially important defect in the exocarp of apple (Malus × domestica), is mainly characterized by the accumulation of suberin on the inner part of the cell wall of the outer epidermal cell layers. However, knowledge on the underlying genetic components triggering this trait remains sketchy. Bulk transcriptomic profiling was performed on the exocarps of three russeted and three waxy apple varieties. This experimental design was chosen to lower the impact of genotype on the obtained results. Validation by qPCR was carried out on representative genes and additional varieties. Gene ontology enrichment revealed a repression of lignin and cuticle biosynthesis genes in russeted exocarps, concomitantly with an enhanced expression of suberin deposition, stress responsive, primary sensing, NAC and MYB-family transcription factors, and specific triterpene biosynthetic genes. Notably, a strong correlation (R2 = 0.976) between the expression of a MYB93-like transcription factor and key suberin biosynthetic genes was found. Our results suggest that russeting is induced by a decreased expression of cuticle biosynthetic genes, leading to a stress response which not only affects suberin deposition, but also the entire structure of the cell wall. The large number of candidate genes identified in this study provides a solid foundation for further functional studies

Virgo: a laser interferometer to detect gravitational waves

This paper presents a complete description of Virgo, the French-Italian gravitational wave detector. The detector, built at Cascina, near Pisa (Italy), is a very large Michelson interferometer, with 3 km-long arms. In this paper, following a presentation of the physics requirements, leading to the specifications for the construction of the detector, a detailed description of all its different elements is given.These include civil engineering infrastructures, a huge ultra-high vacuum (UHV) chamber (about 6000 cubic metres), all of the optical components, including high quality mirrors and their seismic isolating suspensions, all of the electronics required to control the interferometer and for signal detection. The expected performances of these different elements are given, leading to an overall sensitivity curve as a function of the incoming gravitational wave frequency. This description represents the detector as built and used in the first data-taking runs. Improvements in different parts have been and continue to be performed, leading to better sensitivities. These will be detailed in a forthcoming paper

Virgo: a laser interferometer to detect gravitational waves

none336sìThis paper presents a complete description of Virgo, the French-Italian gravitational wave detector. The detector, built at Cascina, near Pisa (Italy), is a very large Michelson interferometer, with 3 km-long arms. In this paper, following a presentation of the physics requirements, leading to the specifications for the construction of the detector, a detailed description of all its different elements is given. These include civil engineering infrastructures, a huge ultra-high vacuum (UHV) chamber (about 6000 cubic metres), all of the optical components, including high quality mirrors and their seismic isolating suspensions, all of the electronics required to control the interferometer and for signal detection. The expected performances of these different elements are given, leading to an overall sensitivity curve as a function of the incoming gravitational wave frequency. This description represents the detector as built and used in the first data-taking runs. Improvements in different parts have been and continue to be performed, leading to better sensitivities. 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N., Colacino; J., Colas; A., Colla; M., Colombini; Conforto, Giovanni; A., Corsi; S., Cortese; F., Cottone; J. P., Coulon; E., Cuoco; S., D'Antonio; G., Daguin; A., Dari; V., Dattilo; P. Y., David; M., Davier; R., Day; G., Debreczeni; G., De Carolis; M., Dehamme; R., Del Fabbro; W., Del Pozzo; M., del Prete; L., Derome; R., De Rosa; R., Desalvo; M., Dialinas; L., Di Fiore; A., Di Lieto; M., Di Paolo Emilio; A., Di Virgilio; A., Dietz; M., Doets; Dominici, Pietro; A., Dominjon; M., Drago; C., Drezen; B., Dujardin; B., Dulach; C., Eder; A., Eleuteri; D., Enard; M., Evans; L., Fabbroni; V., Fafone; H., Fang; I., Ferrante; F., Fidecaro; I., Fiori; R., Flaminio; D., Forest; L. A., Forte; J. D., Fournier; L., Fournier; J., Franc; O., Francois; S., Frasca; F., Frasconi; A., Freise; A., Gaddi; M., Galimberti; L., Gammaitoni; P., Ganau; C., Garnier; F., Garufi; M. 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M., Mackowski; T., Maiani; E., Majorana; C., Magazzù; I., Maksimovic; V., Malvezzi; N., Man; S., Mancini; B., Mansoux; M., Mantovani; F., Marchesoni; F., Marion; P., Marin; J., Marque; Martelli, Filippo; A., Masserot; L., Massonnet; G., Matone; L., Matone; M., Mazzoni; F., Menzinger; C., Michel; L., Milano; Y., Minenkov; S., Mitra; M., Mohan; J. L., Montorio; R., Morand; F., Moreau; J., Moreau; N., Morgado; A., Morgia; S., Mosca; V., Moscatelli; B., Mours; P., Mugnier; F. A., Mul; L., Naticchioni; I., Neri; F., Nocera; E., Pacaud; G., Pagliaroli; A., Pai; L., Palladino; C., Palomba; F., Paoletti; R., Paoletti; A., Paoli; S., Pardi; G., Parguez; M., Parisi; A., Pasqualetti; R., Passaquieti; D., Passuello; M., Perciballi; Perniola, Bruna; G., Persichetti; S., Petit; M., Pichot; Piergiovanni, Francesco; M., Pietka; R., Pignard; L., Pinard; R., Poggiani; P., Popolizio; T., Pradier; M., Prato; G. A., Prodi; M., Punturo; P., Puppo; K., Qipiani; O., Rabaste; D. 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