Genetius

The study uses an optogenetic ChannelRhodopsin 2 variant (XXM2.0) to generate defined cytosolic Ca²⁺ transients in Arabidopsis root cells, revealing that these Ca²⁺ signatures suppress auxin‑induced membrane depolarization, Ca²⁺ spikes, and auxin‑responsive transcription, leading to reversible inhibition of cell division and elongation. This demonstrates that optogenetically imposed Ca²⁺ signals act as dynamic regulators of auxin sensitivity in roots.

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.

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 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 identifies GyrB3 as a novel nuclear factor that interacts with histone deacetylases to regulate transposable element silencing in plants, acting as a suppressor of IBM1 deficiency–induced epigenetic defects. Loss of GyrB3 reduces DNA methylation and increases H3 acetylation at TEs, demonstrating the importance of histone deacetylation for genome stability.

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 introduces a CRISPR/Cas9‑based restoration system (CiRBS) that reactivates a disabled luciferase reporter (LUC40Ins26bp) in transgenic Arabidopsis, enabling long‑term single‑cell bioluminescence monitoring. Restoration occurs within 24 h after particle‑bombardment‑mediated CRISPR delivery, with ~7 % of cells regaining luminescence and most restored cells carrying a single correctly edited chromosome, facilitating reliable analysis of cellular gene‑expression heterogeneity.

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 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.