Biology subjects

latrasse, D.

Publications and source records attributed to latrasse, D..

4 recordsLinked to original sources

bioRxiv2026

A molecular framework of chromatin extrusion in plants

Three-dimensional genome organization is a fundamental regulator of gene expression, yet the mechanisms shaping higher-order chromatin folding in plants remain poorly defined. Here, we identify the Arabidopsis cohesin regulator PDS5A as a central modulator of chromatin loop extrusion and topologically associating domain (TAD)-like architecture. Using Hi-C and Micro-C, we show that loss of PDS5A strongly enhances TAD-like domains and nucleosome-scale stripes and loops across chromosome arms, while leaving large-scale compartmentalization largely intact and revealing conserved TAD-like patterns across tissues and ploidy levels. Genetic analyses indicate that Arabidopsis TAD-like domain formation relies on the plant-specific kleisin SYN4 and is antagonized by WAPL1/2, with PDS5A acting as the dominant cohesin-unloading factor that limits loop extension. Biochemical experiments demonstrate that PDS5A physically associates with cohesin and that its function in suppressing TAD-like domains is independent of direct Tudor domain-mediated binding to H3K4me1-marked chromatin. Micro-C further resolves that chromatin loop and stripe anchors formed in pds5a are highly enriched at accessible, strongly transcribed promoters and are marked by the plant site II motif TGGGCC/T, implicating site II-binding transcription factors as plant-specific boundary elements analogous to CTCF in animals. Finally, mutational disruption of distal chromatin anchors shows that newly formed chromatin contacts in pds5a can act as cis-regulatory modules that influence target gene expression. Together, these findings identify a PDS5A-regulated chromatin extrusion module that shapes plant 3D genome architecture and uncover a promoter- and motif-based logic for loop anchoring and transcriptional control in plants.

genomics↗

bioRxiv2023

Genome-wide evidence of the role of Paf1C in transcription elongation and histone H2B monoubiquitination in Arabidopsis

The evolutionarily conserved Paf1 complex (Paf1C) participates in transcription, and research in animals and fungi suggests that it facilitates RNAPII progression through chromatin remodeling. To obtain evidence that Paf1C acts in transcription elongation in Arabidopsis, we examined the genomic distribution of the ELF7 and VIP3 subunits of Paf1C. The occupancy of both subunits was confined to thousands of gene bodies and positively correlated with RNAPII occupancy and the level of gene expression, supporting a role as a transcription elongation factor. We found that monoubiquitinated histone H2B, which marks most transcribed genes, was strongly reduced genome-wide in elf7 seedlings. Genome-wide profiling of RNAPII revealed that in elf7 mutants, RNAPII occupancy was reduced throughout the gene body and at the transcription end site of Paf1C-targeted genes, suggesting a direct role for the complex in transcription elongation. Overall, our observations suggest that there is a direct functional link between Paf1C activity, mono-ubiquitination of histone H2B, and the transition of RNPII to productive elongation. However, for several genes, Paf1C may also act independently of H2Bub deposition or occupy these genes more stably than H2Bub marking, possibly reflecting the dynamic nature of Paf1C association and H2Bub turnover during transcription.

plant biology↗

bioRxiv2023

The CRL plastid outer envelope protein supports TOC75-V / OEP80 complex formation in Arabidopsis

Embedded {beta}-barrel proteins in the outer envelope membrane mediate most cellular traffic between the cytoplasm and the plastids. Although TOC75-V/OEP80 has been implicated in the insertion and assembly of {beta}-barrel proteins in the outer envelope membrane of Arabidopsis thaliana, relatively little is known about this process. CRUMPLED LEAF (CRL) encodes a protein localizing in the outer envelope membrane, and its loss of function results in pleiotropic defects, including altered plant morphogenesis, growth retardation, suppression of plastid division, and spontaneous light intensity-dependent localized cell death. A suppressor screen conducted on mutagenized crl mutants with ethyl methanesulfonate revealed that a missense mutation in OEP80 suppresses crls pleiotropic defects. Furthermore, we found that the complex formation of OEP80 was compromised in crl. Furthermore, we demonstrated that CRL interacts with OEP80 in vivo and that a portion of CRL is present in protein complexes with the same molecular weight as the OEP80-associated complex. Our results suggest that CRL interacts with OEP80 to regulate its complex formation. CRL has been shown to be involved in plastid protein import; therefore, pleiotropic defects in crl are likely due to the combined effects of decreased plastid protein import and altered membrane integration of {beta}-barrel proteins in the outer envelope membrane. This study sheds light on the mechanisms that allow the integration of {beta}-barrel proteins into the outer envelope membrane of plastids and the significance of this finding for plant cellular processes.

plant biology↗

bioRxiv2023

Distinctive and complementary roles of E2F transcription factors during plant replication stress response

Survival of living organisms is fully dependent on their maintenance of genome integrity, being permanently threatened by replication stress in proliferating cells. Although the plant DNA damage response (DDR) regulator SOG1 has been demonstrated to cope with replicative defects, accumulating evidence points to other pathways functioning independently of SOG1. Here, we have studied the role of the Arabidopsis E2FA and EF2B transcription factors, two well-characterized regulators of DNA replication, in the response to replication stress. Through a combination of reverse genetics and chromatin-immunoprecipitation approaches, we show that E2FA and E2FB share many target genes with SOG1, providing evidence for their involvement in the DDR. Analysis of double and triple mutant combinations revealed that E2FB, rather than E2FA, plays the most prominent role in sustaining growth in the presence of replicative defects, either operating antagonistically or synergistically with SOG1. Reversely, SOG1 aids in overcoming the replication defects of E2FA/E2FB-deficient plants. Our data reveal a complex transcriptional network controlling the replication stress response, in which both E2Fs and SOG1 act as key regulatory factors. ONE-SENTENCE SUMMARYThe Arabidopsis E2FA and EF2B transcription factors differently contribute to the plants response to DNA replication defects in a cooperative way with the DNA damage response regulator SOG1.

genetics↗