Wheat TaPUB1 Regulates Cd Uptake and Tolerance by Promoting the Degradation of TaIRT1 and TaIAA17.

Cadmium (Cd) accumulation in agricultural soils is an increasingly serious problem, as plants absorb Cd, which inhibits their growth and development. Nonetheless, the molecular mechanisms underlying Cd detoxification and accumulation in wheat (Triticum aestivum L.) are unclear. Here, we isolated the U-box E3 ligase TaPUB1 from wheat and reported the functional characterization of TaPUB1 in Cd uptake and tolerance in wheat. Under Cd stress, TaPUB1 overexpression lines displayed higher photosynthetic rates than the wild type; opposite results were observed in the TaPUB1-RNAi lines. In addition, TaPUB1 overexpression lines showed reduced Cd uptake and accumulation, whereas RNAi plants exhibited a significant increase in Cd accumulation after Cd treatment. We further found that TaPUB1 enhanced the resistance of wheat to Cd stress in three ways. First, TaPUB1 interacts with and ubiquitinates TaIRT1, resulting in the inhibition of Cd uptake. Second, TaPUB1 interacts directly with and ubiquitinates TaIAA17, facilitates its degradation, and results in primary root elongation by activating the Aux signaling pathway under Cd stress. Moreover, TaPUB1 decreases ROS accumulation by regulating antioxidant-related gene expression and antioxidant enzyme activity under Cd stress. Thus, a molecular mechanism by which TaPUB1 regulates Cd uptake and tolerance by modulating the stability of TaIRT1 and TaIAA17 proteins was revealed.

A polysaccharide deacetylase from Puccinia striiformis f. sp. tritici is an important pathogenicity gene that suppresses plant immunity.

The cell wall of filamentous fungi, comprised of chitin, polysaccharide and glycoproteins, maintains the integrity of hyphae and protect them from defence responses by potential host plants. Here, we report that one polysaccharide deacetylase of Puccinia striiformis f. sp. tritici (Pst), Pst_13661, suppresses Bax-induced cell death in plants and Pst_13661 is highly induced during early stages of the interaction between wheat and Pst. Importantly, the transgenic wheat expressing the RNA interference (RNAi) construct of Pst_13661 exhibits high resistance to major Pst epidemic races CYR31, CYR32 and CYR33 by inhibiting growth and development of Pst, indicating that Pst_13661 is an available pathogenicity factor and is a potential target for generating broad-spectrum resistance breeding material of wheat. It forms a homo-polymer and has high affinity for chitin and germ tubes of Pst compared with the control. Besides, Pst_13661 suppresses chitin-induced plant defence in plants. Hence, we infer that Pst_13661 may modify the fungal cell wall to prevent recognition by apoplastic surveillance systems in plants. This study opens new approaches for developing durable disease-resistant germplasm by disturbing the growth and development of fungi and develops novel strategies to control crop diseases.

YR36/WKS1-Mediated Phosphorylation of PsbO, an Extrinsic Member of Photosystem II, Inhibits Photosynthesis and Confers Stripe Rust Resistance in Wheat.

Wheat stripe rust, due to infection by Puccinia striiformis f. sp. tritici (Pst), is a devastating disease that causes significant global grain yield losses. Yr36, which encodes Wheat Kinase START1 (WKS1), is an effective high-temperature adult-plant resistance gene and confers resistance to a broad spectrum of Pst races. We previously showed that WKS1 phosphorylates the thylakoid ascorbate peroxidase protein and reduces its ability to detoxify peroxides, which may contribute to the accumulation of reactive oxygen species (ROS). WKS1-mediated Pst resistance is accompanied by leaf chlorosis in Pst-infected regions, but the underlying mechanisms remain elusive. Here, we show that WKS1 interacts with and phosphorylates PsbO, an extrinsic member of photosystem II (PSII), to reduce photosynthesis, regulate leaf chlorosis, and confer Pst resistance. A point mutation in PsbO-A1 or reduction in its transcript levels by RNA interference resulted in chlorosis and reduced Pst sporulation. Biochemical analyses revealed that WKS1 phosphorylates PsbO at two conserved amino acids involved in physical interactions with PSII and reduces the binding affinity of PsbO with PSII. Presumably, phosphorylated PsbO proteins dissociate from the PSII complex and then undergo rapid degradation by cysteine and aspartic proteases. Taken together, these results demonstrate that perturbations of wheat PsbO by point mutation or phosphorylation by WKS1 reduce the rate of photosynthesis and delay the growth of Pst pathogen before the induction of ROS.

An ancestral NB-LRR with duplicated 3'UTRs confers stripe rust resistance in wheat and barley.

Wheat stripe rust, caused by Puccinia striiformis f. sp. tritici (Pst), is a global threat to wheat production. Aegilops tauschii, one of the wheat progenitors, carries the YrAS2388 locus for resistance to Pst on chromosome 4DS. We reveal that YrAS2388 encodes a typical nucleotide oligomerization domain-like receptor (NLR). The Pst-resistant allele YrAS2388R has duplicated 3' untranslated regions and is characterized by alternative splicing in the nucleotide-binding domain. Mutation of the YrAS2388R allele disrupts its resistance to Pst in synthetic hexaploid wheat; transgenic plants with YrAS2388R show resistance to eleven Pst races in common wheat and one race of P. striiformis f. sp. hordei in barley. The YrAS2388R allele occurs only in Ae. tauschii and the Ae. tauschii-derived synthetic wheat; it is absent in 100% (n = 461) of common wheat lines tested. The cloning of YrAS2388R will facilitate breeding for stripe rust resistance in wheat and other Triticeae species.

A novel compound heterozygous mutations in protein C gene causing neonatal purpura fulminans.

: Neonatal purpura fulminans is a rare, life-threatening disease caused by severe congenital deficiency of protein C (PC) because of homozygous or compound heterozygous mutations in the PROC gene. Mutation analysis plays a critical role in diagnosing the disorder and offering prenatal guidance. In this study, we identified a genetic defect in the PROC gene leading to neonatal purpura fulminans. The propositus had very low PC activity (4%) and PC antigen activity (5%). DNA screening of the whole PROC gene revealed two compound heterozygous mutations in exon8 (c.795_796insA) and exon9 (c.1206_1207insG). These two variations led to the compound heterozygous mutations of Gly266Argfs4 and Pro405Alafs20, which were inherited from the patient's father and mother, respectively. His older sister is heterozygous for the Gly266Argfs4 mutation. The inserted nucleotides alter the protein by introducing a stop codon at the subsequent AA position, resulting in a truncated protein compared with the wild type. We deduced that the compound heterozygous mutations are responsible for the PC deficiency, the Gly266Argfs4 mutation has been confirmed to be a novel mutation.