@article{han_hung_zhang_bartels_rea_yang_park_zhang_fischer_xiao_et al._2022, title={Loss of linker histone H1 in the maternal genome influences DEMETER-mediated demethylation and affects the endosperm DNA methylation landscape}, volume={13}, ISSN={["1664-462X"]}, DOI={10.3389/fpls.2022.1070397}, abstractNote={The Arabidopsis DEMETER (DME) DNA glycosylase demethylates the central cell genome prior to fertilization. This epigenetic reconfiguration of the female gamete companion cell establishes gene imprinting in the endosperm and is essential for seed viability. DME demethylates small and genic-flanking transposons as well as intergenic and heterochromatin sequences, but how DME is recruited to these loci remains unknown. H1.2 was identified as a DME-interacting protein in a yeast two-hybrid screen, and maternal genome H1 loss affects DNA methylation and expression of selected imprinted genes in the endosperm. Yet, the extent to which H1 influences DME demethylation and gene imprinting in the Arabidopsis endosperm has not been investigated. Here, we showed that without the maternal linker histones, DME-mediated demethylation is facilitated, particularly in the heterochromatin regions, indicating that H1-bound heterochromatins are barriers for DME demethylation. Loss of H1 in the maternal genome has a very limited effect on gene transcription or gene imprinting regulation in the endosperm; however, it variably influences euchromatin TE methylation and causes a slight hypermethylation and a reduced expression in selected imprinted genes. We conclude that loss of maternal H1 indirectly influences DME-mediated demethylation and endosperm DNA methylation landscape but does not appear to affect endosperm gene transcription and overall imprinting regulation.}, journal={FRONTIERS IN PLANT SCIENCE}, author={Han, Qiang and Hung, Yu-Hung and Zhang, Changqing and Bartels, Arthur and Rea, Matthew and Yang, Hanwen and Park, Christine and Zhang, Xiang-Qian and Fischer, Robert L. L. and Xiao, Wenyan and et al.}, year={2022}, month={Dec} } @article{pecorelli_cordone_messano_zhang_falone_amicarelli_hayek_valacchi_2020, title={Altered inflammasome machinery as a key player in the perpetuation of Rett syndrome oxinflammation}, volume={28}, ISSN={["2213-2317"]}, DOI={10.1016/j.redox.2019.101334}, abstractNote={Rett syndrome (RTT) is a progressive neurodevelopmental disorder mainly caused by mutations in the X-linked MECP2 gene. RTT patients show multisystem disturbances associated with an oxinflammatory status. Inflammasomes are multi-protein complexes, responsible for host immune responses against pathogen infections and redox-related cellular stress. Assembly of NLRP3/ASC inflammasome triggers pro-caspase-1 activation, thus, resulting in IL-1β and IL-18 maturation. However, an aberrant activation of inflammasome system has been implicated in several human diseases. Our aim was to investigate the possible role of inflammasome in the chronic subclinical inflammatory condition typical of RTT, by analyzing this complex in basal and lipopolysaccharide (LPS)+ATP-stimulated primary fibroblasts, as well as in serum from RTT patients and healthy volunteers. RTT cells showed increased levels of nuclear p65 and ASC proteins, pro-IL-1β mRNA, and NLRP3/ASC interaction in basal condition, without any further response upon the LPS + ATP stimuli. Moreover, augmented levels of circulating ASC and IL-18 proteins were found in serum of RTT patients, which are likely able to amplify the inflammatory response. Taken together, our findings suggest that RTT patients exhibited a challenged inflammasome machinery at cellular and systemic level, which may contribute to the subclinical inflammatory state feedback observed in this pathology.}, journal={REDOX BIOLOGY}, author={Pecorelli, Alessandra and Cordone, Valeria and Messano, Nicolo and Zhang, Changqing and Falone, Stefano and Amicarelli, Fernanda and Hayek, Joussef and Valacchi, Giuseppe}, year={2020}, month={Jan} } @article{kirkbride_lu_zhang_mosher_baulcombe_chen_2019, title={Maternal small RNAs mediate spatial-temporal regulation of gene expression, imprinting, and seed development in Arabidopsis}, volume={116}, ISSN={["0027-8424"]}, DOI={10.1073/pnas.1807621116}, abstractNote={ Arabidopsis seed development involves maternal small interfering RNAs (siRNAs) that induce RNA-directed DNA methylation (RdDM) through the NRPD1 -mediated pathway. To investigate their biological functions, we characterized siRNAs in the endosperm and seed coat that were separated by laser-capture microdissection (LCM) in reciprocal genetic crosses with an nrpd1 mutant. We also monitored the spatial-temporal activity of the NRPD1 -mediated pathway on seed development using the AGO4:GFP::AGO4 (promoter:GFP::protein) reporter and promoter:GUS sensors of siRNA-mediated silencing. From these approaches, we identified four distinct groups of siRNA loci dependent on or independent of the maternal NRPD1 allele in the endosperm or seed coat. A group of maternally expressed NRPD1 -siRNA loci targets endosperm-preferred genes, including those encoding AGAMOUS-LIKE (AGL) transcription factors. Using translational promoter:AGL::GUS constructs as sensors, we demonstrate that spatial and temporal expression patterns of these genes in the endosperm are regulated by the NRPD1 -mediated pathway irrespective of complete silencing ( AGL91 ) or incomplete silencing ( AGL40 ) of these target genes. Moreover, altered expression of these siRNA-targeted genes affects seed size. We propose that the corresponding maternal siRNAs could account for parent-of-origin effects on the endosperm in interploidy and hybrid crosses. These analyses reconcile previous studies on siRNAs and imprinted gene expression during seed development. }, number={7}, journal={PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA}, author={Kirkbride, Ryan C. and Lu, Jie and Zhang, Changqing and Mosher, Rebecca A. and Baulcombe, David C. and Chen, Z. Jeffrey}, year={2019}, month={Feb}, pages={2761–2766} }