Phosphite (Phi) and phosphate (Pi) share the same root uptake system, but Phi acts as a biostimulant that modulates plant growth and disease resistance in a species‑ and Pi‑dependent manner. In Arabidopsis, Phi induces hypersensitive‑like cell death and enhances resistance to Plectosphaerella cucumerina, while in rice it counteracts Pi‑induced susceptibility to Magnaporthe oryzae and Fusarium fujikuroi, accompanied by extensive transcriptional reprogramming.
The study created a system that blocks root‑mediated signaling between wheat varieties in a varietal mixture and used transcriptomic and metabolomic profiling to reveal that root chemical interactions drive reduced susceptibility to Septoria tritici blotch, with phenolic compounds emerging as key mediators. Disruption of these root signals eliminates both the disease resistance phenotype and the associated molecular reprogramming.
The study investigates the role of the chromatin regulator MpSWI3, a core subunit of the SWI/SNF complex, in the liverwort Marchantia polymorpha. A promoter mutation disrupts male gametangiophore development and spermiogenesis, causing enhanced vegetative propagation, and transcriptomic analysis reveals that MpSWI3 regulates genes controlling reproductive initiation, sperm function, and asexual reproduction, highlighting its ancient epigenetic role in balancing vegetative and reproductive phases.
Using genome‑wide association studies in Arabidopsis thaliana, the authors identified the chromatin‑associated protein CDCA7 as a trans‑regulator that specifically controls CG methylation (mCG) and TE silencing. CDCA7 and its paralog CDCA7β bind the remodeler DDM1, modulating its activity without broadly affecting non‑CG methylation or histone variant deposition, and natural variation in CDCA7 regulatory sequences correlates with local ecological adaptation.
The study presents an optimized Agrobacterium-mediated transformation protocol for bread wheat that incorporates a GRF4‑GIF1 fusion to enhance regeneration and achieve genotype‑independent transformation across multiple cultivars. The approach consistently improves transformation efficiency while limiting pleiotropic effects, offering a versatile platform for functional genomics and gene editing in wheat.
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.
The study examines how the SnRK1 catalytic subunit KIN10 integrates carbon availability with root growth regulation in Arabidopsis thaliana. Loss of KIN10 reduces glucose‑induced inhibition of root elongation and triggers widespread transcriptional reprogramming of metabolic and hormonal pathways, notably affecting auxin and jasmonate signaling under sucrose supplementation. These findings highlight KIN10 as a central hub linking energy status to developmental and environmental cues in roots.
The study shows that silencing of NOR2 rRNA genes in Arabidopsis thaliana depends primarily on CHH-context cytosine methylation, particularly mediated by CMT2 and the chromatin remodeler DDM1, rather than CG or CHG methylation. Comparative promoter analysis revealed a prevalence of CHH sites in plant rDNA promoters, explaining why CHH methylation mutants disrupt NOR2 silencing more strongly, while NOR2 loci are hyper‑methylated and more condensed than NOR4.