Genetius

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 applied a progressive, sublethal drought treatment to Arabidopsis thaliana, collecting time‑resolved phenotypic and transcriptomic data. Machine‑learning analysis revealed distinct drought stages driven by multiple overlapping transcriptional programs that intersect with plant aging, and identified high‑explanatory‑power transcripts as biomarkers rather than causal agents.

The study shows that inoculating Arabidopsis thaliana with the plant‑growth‑promoting bacterium Enterobacter sp. SA187 markedly boosts root and shoot biomass under elevated CO₂, accompanied by altered nitrogen and carbon content and reshaped phytohormone signaling. Transcriptomic and metabolomic analyses reveal activation of salicylic acid, jasmonic acid, and ethylene pathways and enhanced primary metabolism, while the ethylene‑insensitive ein2‑1 mutant demonstrates that the growth benefits are ethylene‑dependent.

The study reveals that the endoplasmic reticulum‑associated degradation (ERAD) pathway governs the proteasome‑dependent turnover of PIN‑LIKES (PILS) auxin transport proteins under normal conditions, and that both internal and external cues modulate this process via the ERAD complex. These findings link ER protein homeostasis to auxin‑mediated growth regulation, highlighting a new mechanism by which plants adapt to environmental and developmental signals.

The study combined cell biology, transcriptomics, and ionomics to reveal that zinc deficiency reduces root apical meristem size while preserving meristematic activity and local Zn levels, leading to enhanced cell elongation and differentiation in Arabidopsis thaliana. ZIP12 was identified as a highly induced gene in the zinc‑deficient root tip, and zip12 mutants displayed impaired root growth, altered RAM structure, disrupted Zn‑responsive gene expression, and abnormal metal partitioning, highlighting ZIP12’s role in maintaining Zn homeostasis and meristem function.

The study used Arabidopsis thaliana mutants with low (vtc2, vtc4) and high (vtc2/OE-VTC2) ascorbate levels to examine how ascorbate concentration affects gene expression and cellular homeostasis. Transcriptomic analysis revealed that altered ascorbate levels modulate defense and stress pathways, and that TAA1/TAR2‑mediated auxin biosynthesis is required for coping with elevated ascorbate in a light‑dependent manner.

The study investigates how auxin regulates root cell elongation in Arabidopsis thaliana by modulating the transcription of pectin‑degrading polygalacturonases (PGRAs). Auxin down‑regulates PGRA1 expression to limit pectin remodeling, and mutants lacking PGRAs fail to enhance root growth when auxin levels are reduced, linking auxin signaling to cell‑wall modification.

The study identifies the serine/threonine protein kinase CIPK14/SNRK3.15 as a regulator of sulfate‑deficiency responses in Arabidopsis thaliana seedlings, with mutants showing diminished early adaptive and later salvage responses under sulfur starvation. While snrk3.15 mutants exhibit no obvious phenotype under sufficient sulfur, the work provides a novel proteomic dataset comparing wild‑type and mutant seedlings under sulfur limitation.

The study reveals that cross‑talk between the ERECTA receptor pathway and auxin signaling determines the output of bilateral stem cell layers during secondary growth by phosphorylating the transcription factor AINTEGUMENTA (ANT). Phosphorylation of ANT biases stem cell activity toward the production of a single vascular cell type, thereby modulating root girth and overall biomass accumulation.

The study identifies TOW as a critical component linking intracellular auxin signaling to cell surface perception, thereby regulating PIN transporter polarity and trafficking during auxin canalization. tow mutants show impaired vascular regeneration and defective PIN polarization, with TOW localizing to Golgi, TGN, and plasma membrane and interacting with TMK1 and the CAMEL-CANAR complex. These findings elucidate how auxin signaling coordinates directional transport for flexible vasculature formation.