Pectin methylesterification state and cell wall mechanical properties contribute to neighbor proximity-induced hypocotyl growth in Arabidopsis

Fabien Sénéchal ^1 2, Sarah Robinson ^3 4, Evert Van Schaik ^5 6, Martine Trévisan ¹, Prashant Saxena ^1 7, Didier Reinhardt ⁵, Christian Fankhauser ¹

. 2024 Apr 21;8(4):e584.

 doi: 10.1002/pld3.584. eCollection 2024 Apr.

• PMID: 38646567
• PMCID: PMC11033045
• DOI: 10.1002/pld3.584

Abstract

Plants growing with neighbors compete for light and consequently increase the growth of their vegetative organs to enhance access to sunlight. This response, called shade avoidance syndrome (SAS), involves photoreceptors such as phytochromes as well as phytochrome interacting factors (PIFs), which regulate the expression of growth-mediating genes. Numerous cell wall-related genes belong to the putative targets of PIFs, and the importance of cell wall modifications for enabling growth was extensively shown in developmental models such as dark-grown hypocotyl. However, the contribution of the cell wall in the growth of de-etiolated seedlings regulated by shade cues remains poorly established. Through analyses of mechanical and biochemical properties of the cell wall coupled with transcriptomic analysis of cell wall-related genes from previously published data, we provide evidence suggesting that cell wall modifications are important for neighbor proximity-induced elongation. Further analysis using loss-of-function mutants impaired in the synthesis and remodeling of the main cell wall polymers corroborated this. We focused on the cgr2cgr3 double mutant that is defective in methylesterification of homogalacturonan (HG)-type pectins. By following hypocotyl growth kinetically and spatially and analyzing the mechanical and biochemical properties of cell walls, we found that methylesterification of HG-type pectins was required to enable global cell wall modifications underlying neighbor proximity-induced hypocotyl growth. Collectively, our work suggests that plant competition for light induces changes in the expression of numerous cell wall genes to enable modifications in biochemical and mechanical properties of cell walls that contribute to neighbor proximity-induced growth.

Enhancer-promoter interactions become more instructive in the transition from cell-fate specification to tissue differentiation

Tim Pollex ^1 2, Adam Rabinowitz ¹, Maria Cristina Gambetta ^1 3, Raquel Marco-Ferreres ¹, Rebecca R Viales ¹, Aleksander Jankowski ^1 4, Christoph Schaub ¹, Eileen E M Furlong ⁵

Affiliations expand

. 2024 Apr;56(4):686-696.

 doi: 10.1038/s41588-024-01678-x. Epub 2024 Mar 11.

• PMID: 38467791
• PMCID: PMC11018526
• DOI: 10.1038/s41588-024-01678-x

Abstract

To regulate expression, enhancers must come in proximity to their target gene. However, the relationship between the timing of enhancer-promoter (E-P) proximity and activity remains unclear, with examples of uncoupled, anticorrelated and correlated interactions. To assess this, we selected 600 characterized enhancers or promoters with tissue-specific activity in Drosophila embryos and performed Capture-C in FACS-purified myogenic or neurogenic cells during specification and tissue differentiation. This enabled direct comparison between E-P proximity and activity transitioning from OFF-to-ON and ON-to-OFF states across developmental conditions. This showed remarkably similar E-P topologies between specified muscle and neuronal cells, which are uncoupled from activity. During tissue differentiation, many new distal interactions emerge where changes in E-P proximity reflect changes in activity. The mode of E-P regulation therefore appears to change as embryogenesis proceeds, from largely permissive topologies during cell-fate specification to more instructive regulation during terminal tissue differentiation, when E-P proximity is coupled to activation.

. 2024 Apr 3:119721.

 doi: 10.1016/j.bbamcr.2024.119721. Online ahead of print.

E2F transcription factor-1 modulates expression of glutamine metabolic genes in mouse embryonic fibroblasts and uterine sarcoma cells

Katharina Huber ¹, Albert Giralt ², René Dreos ², Helene Michenthaler ³, Sarah Geller ², Valentin Barquissau ², Dorian V Ziegler ², Daniele Tavernari ⁴, Hector Gallart-Ayala ⁵, Katarina Krajina ⁶, Katharina Jonas ⁶, Giovanni Ciriello ⁴, Julijana Ivanisevic ⁵, Andreas Prokesch ⁷, Martin Pichler ⁸, Lluis Fajas ⁹

Affiliations expand

• PMID: 38580088
• DOI: 10.1016/j.bbamcr.2024.119721

Abstract

Metabolic reprogramming is considered as a hallmark of cancer and is clinically exploited as a novel target for therapy. The E2F transcription factor-1 (E2F1) regulates various cellular processes, including proliferative and metabolic pathways, and acts, depending on the cellular and molecular context, as an oncogene or tumor suppressor. The latter is evident by the observation that E2f1-knockout mice develop spontaneous tumors, including uterine sarcomas. This dual role warrants a detailed investigation of how E2F1 loss impacts metabolic pathways related to cancer progression. Our data indicate that E2F1 binds to the promoter of several glutamine metabolism-related genes. Interestingly, the expression of genes in the glutamine metabolic pathway were increased in mouse embryonic fibroblasts (MEFs) lacking E2F1. In addition, we confirm that E2f1^-/- MEFs are more efficient in metabolizing glutamine and producing glutamine-derived precursors for proliferation. Mechanistically, we observe a co-occupancy of E2F1 and MYC on glutamine metabolic promoters, increased MYC binding after E2F1 depletion and that silencing of MYC decreased the expression of glutamine-related genes in E2f1^-/- MEFs. Analyses of transcriptomic profiles in 29 different human cancers identified uterine sarcoma that showed a negative correlation between E2F1 and glutamine metabolic genes. CRISPR/Cas9 knockout of E2F1 in the uterine sarcoma cell line SK-UT-1 confirmed elevated glutamine metabolic gene expression, increased proliferation and increased MYC binding to glutamine-related promoters upon E2F1 loss. Together, our data suggest a crucial role of E2F1 in energy metabolism and metabolic adaptation in uterine sarcoma cells.