GUN2 and GUN3 Coordinate Heme and Chlorophyll Metabolism Thereby Impacting Singlet Oxygen Production and Photooxidative Responses.

YGL46 encoding ferredoxin-like protein interacts with FTR and CAO to regulate chlorophyll synthesis and leaf development in maize.

Chlorophyll is crucial in photosynthesis, enabling plants to absorb light energy for photosynthesis. Here, we identified a yellow-green leaf mutant ygl46 derived from natural variation. Phenotypic characterization exhibited pale leaves. In the mutant, chlorophyll accumulation was significantly reduced, especially chlorophyll b. The mutated phenotype is governed by a single recessive gene. The mutation site was mapped to a 270-kb physical interval between the Indel markers ID0270 and ID0302 on chromosome 5 using an F2 mapping population. A gene (Zm00001d013534) encoding ferredoxin-like (FdC2) protein with varied expression pattern was identified as the candidate gene. The precursor protoporphyrin IX (Proto IX) accumulated to higher levels, while downstream intermediates including Mg-protoporphyrin IX (MgP IX) and protochlorophyllide (Pchlide) were significantly decreased. Functional analysis showed that YGL46 interacts with ferredoxin-thioredoxin reductase (ZmFTR, Zm00001d045366), potentially functioning as an electron donor, to affect MgP IX accumulation, thereby regulating leaf development. In addition, YGL46 interacts with chlorophyllide a oxygenase (ZmCAO, Zm00001d002408) to regulate chlorophyll b (Chl b) biosynthesis.

OXR2 integrates UV-B photomorphogenic signalling, DNA repair, cell cycle regulation, and phenolic compound accumulation in Arabidopsis thaliana.

Ultraviolet-B radiation has a dual effect on plants, acting both as a developmental cue and a source of genetic stress. Plants must balance growth, DNA repair, cell division, and damage mitigation. Oxidation Resistance (OXR) proteins are evolutionarily conserved, TLDc-domain-containing mitochondrial proteins that link redox homeostasis to nuclear stress responses, which makes them strong candidates to coordinate the plant response to UV-B. This study highlights that the Arabidopsis protein AtOXR2 and its sunflower orthologue, HaOXR2, are critical for enhancing plant tolerance to UV-B radiation. Transgenic plants overexpressing AtOXR2 or HaOXR2 showed improved growth under UV-B radiation, with reduced inhibition of leaf, hypocotyl, and root development. Additionally, these plants exhibited reduced meristematic cell death and fewer cyclobutane pyrimidine dimers, a major form of UV-B-induced DNA damage. In vivo analysis using the PlaCCI reporter revealed that while wild-type plants arrest in the G2/M phase after UV-B, OXR2-overexpressing lines maintain a G1/S-enriched cell-cycle profile, suggesting reduced perception of UV-B damage. Furthermore, these plants showed elevated expression of genes associated with light signalling, DNA repair, and cell-cycle checkpoints, along with increased accumulation of protective phenolic and flavonoid compounds. Loss-of-function oxr2 mutants did not show reduced UV-B sensitivity, likely due to compensatory upregulation of compensatory mechanisms involving other OXR family members. Comparative transcriptomic analyses support a two-module model where OXR2 pre-activates the canonical UV-B damage response, thereby establishing OXR2 as an agronomic determinant of UV-B tolerance.

Transcriptomic and predictive modeling reveal photosynthetic and stress responses associated with ALAD silencing in citrus

Loss of the plastidial hexokinase CsHXK3 triggers metabolic starvation and ROS imbalance leading to pollen abortion in cucumber.

It is indicated that CsHXK3 may coordinate carbohydrate metabolism with ROS homeostasis during pollen development, offering insights into the metabolic regulation of male reproductive success in plants.

MYB28 and MYB29 transcription factors regulate iron homeostasis and iron-mobilizing coumarin biosynthesis in Arabidopsis thaliana

Iron (Fe) deficiency is a major constraint for plant growth and triggers extensive physiological and transcriptional reprogramming to maintain Fe homeostasis. Here, we identify the glucosinolate-associated transcription factors MYB28 and MYB29 as previously unrecognized regulators of Arabidopsis thaliana adaptation to Fe deficiency. Across various growth systems, loss of MYB28 increased sensitivity to Fe deficiency, whereas the myb28myb29 double mutant displayed stronger chlorosis, reduced root growth and impaired biomass accumulation, indicating cooperative but unequal functions of these transcription factors. Despite their enhanced Fe-deficiency phenotype, double mutant plants accumulated higher Fe levels in roots and exhibited stronger induction of canonical Fe-deficiency responses, suggesting impaired Fe utilization or distribution. RNA-seq revealed extensive transcriptional reprogramming under Fe deficiency, with pronounced deregulation of genes involved in Fe homeostasis, redox processes and growth, particularly in the double mutant. Among these, SCOPOLETIN 8-HYDROXYLASE (S8H) emerged as a major target gene of MYB28. The expression of S8H was almost abolished in myb28 and myb28myb29 mutants, whereas expression of other coumarin biosynthetic genes remained largely unaffected. Promoter activation assays demonstrated that MYB28 activates the S8H promoter, and metabolic analyses showed accumulation of scopolin together with reduced fraxin levels in the mutants, consistent with impaired S8H activity. Collectively, our results identify MYB28 as a key regulator linking specialized metabolism to Fe homeostasis through control of coumarin biosynthesis, thereby expanding the biological functions of MYB28 and MYB29 transcription factors.

OsCYP51H9 integrates brassinosteroid biosynthesis and nitrogen sensing to enhance grain development and nitrogen utilization in rice.

The results suggest that OsCYP51H9 participates in the phytosterol-BR pathway and plays a positive role in rice adaptation to low-nitrogen environments, providing a potential target for molecular breeding.