Cadmium (Cd 2+ ) is a common toxic heavy metal ion. We investigated the roles of hydrogen sulfide (H 2 S) and cysteine (Cys) in plant responses to Cd 2+ stress. The expression of H 2 S synthetic genes LCD and DES1 were induced by Cd 2+ within 3 h, and endogenous H 2 S was then rapidly released. H 2 S promoted the expression of Cys synthesis-related genes SAT1 and OASA1, which led to endogenous Cys accumulation. The H 2 S and Cys cycle system was stimulated by Cd 2+ stress, and it maintained high levels in plant cells. H 2 S inhibited the ROS burst by inducing alternative respiration capacity (AP) and antioxidase activity. H 2 S weakened Cd 2+ toxicity by inducing the metallothionein (MTs) genes expression. Cys promoted GSH accumulation and inhibited the ROS burst, and GSH induced the expression of phytochelatin (PCs) genes, counteracting Cd 2+ toxicity. In summary, the H 2 S and Cys cycle system played a key role in plant responses to Cd 2+ stress. The Cd 2+ tolerance was weakened when the cycle system was blocked in lcddes1-1 and oasa1 mutants. This paper is the first to describe the role of the H 2 S and Cys cycle system in Cd 2+ stress and to explore the relevant and specificity mechanisms of H 2 S and Cys in mediating Cd 2+ stress.Cadmium (Cd 2+ ) is a common toxic heavy metal ion in the environment. It greatly affects the growth and development of plants and is harmful to human health through the food chain 1,2 . Because of its carcinogenic properties and its detrimental effects on the growth of organisms, Cd 2+ contamination of agricultural soil has become a critical concern. Preventing reduced growth and accumulation of Cd 2+ in harvested organs of plants growing on Cd 2+ -contaminated soils has become an urgent task as it can contribute to food safety. Thus, it is important to explore plant stress defense mechanisms and to find ways to reduce the Cd 2+ accumulation in grains.As a heavy metal not participating in redox reactions, Cd 2+ can easily dissolve in water and quickly be taken up by plant roots 3,4 . The physiological consequences of Cd 2+ toxicity in plants are chlorosis, stunted growth, and cell death, among others [5][6][7] . At the cellular level, Cd 2+ can alter protein structure and inhibit enzyme activity by binding to sulfhydryl and carbonyl groups and replacing essential co-factors of enzymes [7][8][9] . The overproduction of reactive oxygen species (ROS) is the primary response of plants to Cd 2+ with negative impact on cell function 10 . Further damage can be caused by ROS-independent, secondary mechanisms. Lipid peroxidation is the most deleterious effect caused by Cd 2+ -induced ROS 4 . Malondialdehyde (MDA), one of the decomposition products of lipid peroxidation, can modify active substrates in plant cells, including nucleic acids, proteins and saccharides 11 . To become resistant to Cd 2+ toxicity, plants have developed several strategies, such as inducing the

Previous studies have revealed the functions of rice and maize AGAMOUS LIKE 6 (AGL6) genes OsMADS6 and ZAG3, respectively, in floral development; however, the functions of three wheat (Triticum aestivum) AGL6 genes are still unclear. Here, we report the main functions of wheat AGL6 homoeologous genes in stamen development. In RNAi plants, stamens showed abnormality in number and morphology, and a tendency to transform into carpels. Consistently, the expression of the B-class gene TaAPETALA3 (AP3) and the auxin-responsive gene TaMGH3 was downregulated, whereas the wheat ortholog of the rice carpel identity gene DROOPING LEAF was ectopically expressed in RNAi stamens. TaAGL6 proteins bind to the promoter of TaAP3 directly. Yeast onehybrid and transient expression assays further showed that TaAGL6 positively regulates the expression of TaAP3 in vivo. Wheat AGL6 transcription factors interact with TaAP3, TaAGAMOUS and TaMADS13. Our findings indicate that TaAGL6 transcription factors play an essential role in stamen development through transcriptional regulation of TaAP3 and other related genes. We propose a model to illustrate the function and probable mechanism of this regulation. This study extends our understanding of AGL6 genes.

Fungal pathogens have evolved combinations of plant cell-wall-degrading enzymes (PCWDEs) to deconstruct host plant cell walls (PCWs). An understanding of this process is hoped to create a basis for improving plant biomass conversion efficiency into sustainable biofuels and bioproducts. Here, an approach integrating enzyme activity assay, biomass pretreatment, field emission scanning electron microscopy (FESEM), and genomic analysis of PCWDEs were applied to examine digestibility or degradability of selected woody and herbaceous biomass by pathogenic fungi. Preferred hydrolysis of apple tree branch, rapeseed straw, or wheat straw were observed by the apple-tree-specific pathogen Valsa mali, the rapeseed pathogen Sclerotinia sclerotiorum, and the wheat pathogen Rhizoctonia cerealis, respectively. Delignification by peracetic acid (PAA) pretreatment increased PCW digestibility, and the increase was generally more profound with non-host than host PCW substrates. Hemicellulase pretreatment slightly reduced or had no effect on hemicellulose content in the PCW substrates tested; however, the pretreatment significantly changed hydrolytic preferences of the selected pathogens, indicating a role of hemicellulose branching in PCW digestibility. Cellulose organization appears to also impact digestibility of host PCWs, as reflected by differences in cellulose microfibril organization in woody and herbaceous PCWs and variation in cellulose-binding domain organization in cellulases of pathogenic fungi, which is known to influence enzyme access to cellulose. Taken together, this study highlighted the importance of chemical structure of both hemicelluloses and cellulose in host PCW digestibility by fungal pathogens.

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