The study demonstrates that the interaction between spliceosomal proteins STA1 and DOT2 controls nuclear speckle organization, pre‑mRNA splicing efficiency, and heat‑stress tolerance in Arabidopsis thaliana. A missense mutation in DOT2 restores the weakened STA1‑DOT2 interaction in the sta1‑1 mutant, linking interaction strength to speckle formation and transcriptome‑wide intron retention under heat stress, while pharmacological inhibition of STA1‑associated speckles reproduces the mutant phenotypes. These findings reveal a heat‑sensitive interaction node that couples spliceosome assembly to nuclear speckle dynamics and splicing robustness.
The study characterizes the chloroplast‑localized protein AT4G33780 in Arabidopsis thaliana using CRISPR/Cas9 knockout and overexpression lines, revealing tissue‑specific expression and context‑dependent effects on seed germination, seedling growth, vegetative development, and root responses to nickel stress. Integrated transcriptomic (RNA‑seq) and untargeted metabolomic analyses show extensive transcriptional reprogramming—especially of cell‑wall genes—and altered central energy metabolism, indicating AT4G33780 coordinates metabolic state with developmental regulation rather than controlling single pathways.
The study identified a heat‑responsive exon‑skipping event in the basic Helix‑Loop‑Helix domain of the transcription factor PIF4, which reduces PIF4 activity and promotes photomorphogenic traits in etiolated seedlings. This reveals a novel post‑transcriptional mechanism by which plants modulate PIF4 function during heat stress.
CLPC2 plays specific roles in CLP complex-mediated regulation of growth, photosynthesis, embryogenesis and response to growth-promoting microbial compounds
Authors: Leal-Lopez, J., Bahaji, A., De Diego, N., Tarkowski, P., Baroja-Fernandez, E., Munoz, F. J., Almagro, G., Perez, C. E., Bastidas-Parrado, L. A., Loperfido, D., Caporalli, E., Ezquer, I., Lopez-Serrano, L., Ferez-Gomez, A., Coca-Ruiz, V., Pulido, P., Morcillo, R. J. L., Pozueta-Romero, J.
The study demonstrates that the plastid chaperone CLPC2, but not its paralogue CLPC1, is essential for Arabidopsis responsiveness to microbial volatile compounds and for normal seed and seedling development. Loss of CLPC2 alters the chloroplast proteome, affecting proteins linked to growth, photosynthesis, and embryogenesis, while overexpression of CLPC2 mimics CLPC1 deficiency, highlighting distinct functional roles within the CLP protease complex.
The study examined DNA methylation dynamics in Arabidopsis thaliana shoots and roots under heat, phosphate deficiency, and combined stress using whole-genome bisulfite sequencing, small RNA‑seq, and RNA‑seq. Distinct stress‑specific methylation patterns were identified, with heat and combined stress causing CHH hypomethylation, phosphate deficiency causing hyper‑ and hypomethylation in shoots and roots respectively, and the combined stress exhibiting a unique signature independent of additive effects. Methylation changes were concentrated in transposable elements and regulatory regions, implicating RdDM and CMT2 pathways and suggesting a role in chromatin accessibility rather than direct transcriptional control.
The study reveals that heat tolerance of meiotic division in Arabidopsis thaliana depends on sustained translation of cell‑cycle genes mediated by the protein TAM, which forms specialized condensates under high temperature. Natural variation was used to identify heat‑sensitive and heat‑tolerant TAM alleles, and boosting TAM translation with complementary peptides rescued heat‑induced meiotic defects, highlighting a potential mechanism driving polyploidisation under climate stress.
Daily Heat Stress Induces Accumulation of Non-functional PSII-LHCII and Donor-side Limitation of PSI via Downregulation of the Cyt bf Complex in Arabidopsis thaliana
The study examined the impact of daily moderate heat stress (38 °C for 4 h) on Arabidopsis thaliana, revealing altered thylakoid ultrastructure and structurally intact but functionally impaired PSII‑LHCII complexes. A pronounced reduction in cytochrome b6f content limited PSI on the donor side, suggesting that Cyt b6f down‑regulation serves as an acclimation mechanism that protects PSI at the expense of overall photosynthetic efficiency.
The study used CRISPR/Cas9 to edit the downstream region of the Arabidopsis thaliana FLOWERING LOCUS T (FT) gene, identifying a 2.3‑kb segment containing the Block E enhancer as crucial for normal FT expression and flowering. Fine‑scale deletions pinpointed a 63‑bp core module with CCAAT‑ and G‑boxes, and revealed a cryptic CCAAT‑box that becomes active when repositioned, highlighting the importance of local chromatin context and motif arrangement for enhancer function.
The study introduces a native‑condition method combining cell fractionation and immuno‑isolation to purify autophagic compartments from Arabidopsis, followed by proteomic and lipidomic characterisation of the isolated phagophore membranes. Proteomic profiling identified candidate proteins linked to autophagy, membrane remodeling, vesicular trafficking and lipid metabolism, while lipidomics revealed a predominance of glycerophospholipids, especially phosphatidylcholine and phosphatidylglycerol, defining the unique composition of plant phagophores.
DECREASE IN DNA METHYLATION 1-mediated epigenetic regulation maintains gene expression balance required for heterosis in Arabidopsis thaliana
Authors: Matsuo, K., Wu, R., Yonechi, H., Murakami, T., Takahashi, S., Kamio, A., Akter, M. A., Kamiya, Y., Nishimura, K., Matsuura, T., Tonosaki, K., Shimizu, M., Ikeda, Y., Kobayashi, H., Seki, M., Dennis, E. S., Fujimoto, R.
The study demonstrates that the chromatin remodeler DDM1 is essential for biomass heterosis in Arabidopsis thaliana hybrids, as loss of DDM1 function leads to reduced rosette growth and extensive genotype‑specific transcriptomic and DNA methylation changes. Whole‑genome bisulfite sequencing revealed widespread hypomethylation in ddm1 mutants, while salicylic acid levels were found unrelated to heterosis, indicating that epigenetic divergence, rather than SA signaling, underpins hybrid vigor.