Phytophthora root rot (PRR), caused by Phytophthora sojae Kaufmann & Gerdemann, is one of the most destructive diseases of soybean [Glycine max (L.) Merr.]. Deployment of resistance genes is the most economical and effective way of controlling the disease. The soybean cultivar 'Yudou 29' is resistant to many P. sojae isolates in China. The genetic basis of the resistance in 'Yudou 29' was elucidated through an inheritance study and molecular mapping. In response to 25 P. sojae isolates, 'Yudou 29' displayed a new resistance reaction pattern distinct from those of differentials carrying known Rps genes. A population of 214 F2:3 families from a cross between 'Jikedou 2' (PRR susceptible) and 'Yudou 29' was used for Rps gene mapping. The segregation fit a ratio of 1:2:1 for resistance:segregation:susceptibility within this population, indicating that resistance in 'Yudou 29' is controlled by a single dominant gene. This gene was temporarily named RpsYD29 and mapped on soybean chromosome 03 (molecular linkage group N; MLG N) flanked by SSR markers SattWM82-50 and Satt1k4b at a genetic distance of 0.5 and 0.2 cM, respectively. Two nucleotide binding site-leucine rich repeat (NBS-LRR) type genes were detected in the 204.8 kb region between SattWM82-50 and Satt1k4b. These two genes showed high similarity to Rps1k in amino acid sequence and could be candidate genes for PRR resistance. Based on the phenotype reactions and the physical position on soybean chromosome 03, RpsYD29 might be a novel allele at, or a novel gene tightly linked to, the Rps1 locus.

A novel er1 allele, er1 -7, conferring pea powdery mildew resistance was characterized by a 10-bp deletion in PsMLO1 cDNA, and its functional marker was developed and validated in pea germplasms. Pea powdery mildew caused by Erysiphe pisi DC is a major disease worldwide. Pea cultivar 'DDR-11' is an elite germplasm resistant to E. pisi. To identify the gene conferring resistance in DDR-11, the susceptible Bawan 6 and resistant DDR-11 cultivars were crossed to produce F1, F2, and F(2:3) populations. The phenotypic segregation patterns in the F2 and F(2:3) populations fit the 3:1 (susceptible:resistant) and 1:2:1 (susceptible homozygotes:heterozygotes:resistant homozygotes) ratios, respectively, indicating that resistance was controlled by a single recessive gene. Analysis of er1-linked markers in the F2 population suggested that the recessive resistance gene in DDR-11 was an er1 allele, which was mapped between markers ScOPE16-1600 and c5DNAmet. To further characterize er1 allele, the cDNA sequences of PsMLO1 from the parents were obtained and a novel er1 allele in DDR-11 was identified and designated as er1-7, which has a 10-bp deletion in position 111-120. The er1-7 allele caused a frame-shift mutation, resulting in a premature termination of translation of PsMLO1 protein. A co-dominant functional marker specific for er1-7 was developed, InDel111-120, which co-segregated with E. pisi resistance in the mapping population. The marker was able to distinguish between pea germplasms with and without the er1-7. Of 161 pea germplasms tested by InDel111-120, seven were detected containing resistance allele er1-7, which was verified by sequencing their PsMLO1 cDNA. Here, a novel er1 allele was characterized and its an ideal functional marker was validated, providing valuable genetic information and a powerful tool for breeding pea resistance to powdery mildew.

Pea powdery mildew, caused by Erysiphe pisi D.C., is an important disease worldwide. Deployment of resistant varieties is the main way to control this disease. This study aimed to screen Chinese pea (Pisum sativum L.) landraces resistant to E. pisi, and to characterize the resistance gene(s) at the er1 locus in the resistant landraces, and to develop functional marker(s) specific to the novel er1 allele. The 322 landraces showed different resistance levels. Among them, 12 (3.73%), 4 (1.24%) and 17 (5.28%) landraces showed immunity, high resistance and resistance to E. pisi, respectively. The other landraces appeared susceptible or highly susceptible to E. pisi. Most of the immune and highly resistant landraces were collected from Yunnan province. To characterize the resistance gene at the er1 locus, cDNA sequences of PsMLO1 gene were determined in 12 immune and four highly resistant accessions. The cDNAs of PsMLO1 from the immune landrace G0005576 produced three distinct transcripts, characterized by a 129-bp deletion, and 155-bp and 220-bp insertions, which were consistent with those of er1-2 allele. The PsMLO1 cDNAs in the other 15 resistant landraces produced identical transcripts, which had a new point mutation (T→C) at position 1121 of PsMLO1, indicating a novel er1 allele, designated as er1-6. This mutation caused a leucine to proline change in the amino acid sequence. Subsequently, the resistance allele er1-6 in landrace G0001778 was confirmed by resistance inheritance analysis and genetic mapping on the region of the er1 locus using populations derived from G0001778 × Bawan 6. Finally, a functional marker specific to er1-6, SNP1121, was developed using the high-resolution melting technique, which could be used in pea breeding via marker-assisted selection. The results described here provide valuable genetic information for Chinese pea landraces and a powerful tool for pea breeders.

The RpsQ Phytophthora resistance locus was finely mapped to a 118-kb region on soybean chromosome 3. A best candidate gene was predicted and three co-segregating gene markers were developed. Phytophthora root rot (PRR), caused by Phytophthora sojae, is a major threat to sustainable soybean production. The use of genetically resistant cultivars is considered the most effective way to control this disease. The Chinese soybean cultivar Qichadou 1 exhibited a broad spectrum resistance, with a distinct resistance phenotype, following inoculation with 36 Chinese P. sojae isolates. Genetic analyses indicated that the disease resistance in Qichadou 1 is controlled by a single dominant gene. This gene locus was designated as RpsQ and mapped to a 118-kb region between BARCSOYSSR_03_0165 and InDel281 on soybean chromosome 3, and co-segregated with Insert11, Insert144 and SNP276. Within this region, there was only one gene Glyma.03g27200 encoding a protein with a typical serine/threonine protein kinase structure, and the expression pattern analysis showed that this gene induced by P. sojae infection, which was suggested as a best candidate gene of RpsQ. Candidate gene specific marker Insert144 was used to distinguish RpsQ from the other known Rps genes on chromosome 3. Identical polymerase chain reaction amplification products were produced for cultivars Qichadou 1 (RpsQ) and Ludou 4 (Rps9). All other cultivars carrying Rps genes on chromosome 3 produced different PCR products, which all lacked a 144-bp fragment present in Qichadou 1 and Ludou 4. The phenotypes of the analyzed cultivars combined with the physical position of the PRR resistance locus, candidate gene analyses, and the candidate gene marker test revealed RpsQ and Rps9 are likely the same gene, and confer resistance to P. sojae.

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Anthracnose is a destructive disease of the common bean (Phaseolus vulgaris L.). The Andean cultivar Hongyundou has been demonstrated to possess strong resistance to anthracnose race 81. To study the genetics of this resistance, the Hongyundou cultivar was crossed with a susceptible genotype Jingdou. Segregation of resistance for race 81 was assessed in the F2 population and F2:3 lines under controlled conditions. Results indicate that Hongyundou carries a single dominant gene for anthracnose resistance. An allele test by crossing Hongyundou with another resistant cultivar revealed that the resistance gene is in the Co-1 locus (therefore named Co-1HY). The physical distance between this locus and the two flanking markers was 46 kb, and this region included four candidate genes, namely, Phvul.001G243500, Phvul.001G243600, Phvul.001G243700 and Phvul.001G243800. These candidate genes encoded serine/threonine-protein kinases. Expression analysis of the four candidate genes in the resistant and susceptible cultivars under control condition and inoculated treatment revealed that all the four candidate genes are expressed at significantly higher levels in the resistant genotype than in susceptible genotype. Phvul.001G243600 and Phvul.001G243700 are expressed nearly 15-fold and 90-fold higher in the resistant genotype than in the susceptible parent before inoculation, respectively. Four candidate genes will provide useful information for further research into the resistance mechanism of anthracnose in common bean. The closely linked flanking markers identified here may be useful for transferring the resistance allele Co-1HY from Hongyundou to elite anthracnose susceptible common bean lines.

Acute pancreatitis (AP) is an acute inflammatory process of the pancreas that is characterized by inflammation, edema, vacuolization and necrosis, which has significant morbidity and lethality. The pathogenesis of AP has not been established completely. An early and critical feature of AP is the aberrant signaling of Calcium (Ca2+) within the pancreatic acinar cell, termed Ca2+ overload. Store-operated Ca2+ (SOC) channels are the principal Ca2+ influx channels that contribute to Ca2+ overload in pancreatic acinar cells. Store-operated Ca2+ entry (SOCE) has been proved to be a key pathogenic step in AP development that leads to trypsin activation, inflammation and vacuolization. However, the molecular mechanisms are still poorly understood. By establishing Ca2+ overload model and mouse AP model using caerulein, we found that caerulein triggered SOCE via inducing interaction between STIM1 and Orai1, which activated calcineurin (CaN); CaN activated the nuclear factor of activated T cells (NFAT) and transcription factor EB (TFEB), thus promoting the transcriptional activation of multiple chemokines genes and autophagy-associated genes respectively. To the best of our knowledge, this is the first evidence showing that SOCE activates TFEB via CaN activation, which may have noticeable longer-term effects on autophagy and vacuolization in AP development. Our findings reveal the role for SOCE/CaN in AP development and provide potential targets for AP treatment.

Two dominant powdery mildew resistance genes introduced from Triticum carthlicum accession PS5 to common wheat were identified and tagged using microsatellite markers. The gene designated PmPS5A was placed on wheat chromosome 2AL and linked to the microsatellite marker Xgwm356 at a genetic distance of 10.2 cM. Based on the information of its origin, chromosome location, and reactions to 5 powdery mildew isolates, this gene could be a member of the complex Pm4 locus. The 2nd gene designated PmPS5B was located on wheat chromosome 2BL with 3 microsatellite markers mapping proximally to the gene: Xwmc317 at 1.1 cM; Xgwm111 at 2.2 cM; and Xgwm382 at 4.0 cM; and 1 marker, Xgwm526, mapping distally to the gene at a distance of 18.1 cM. Since this gene showed no linkage to the other 2 known powdery mildew resistance genes on wheat chromosome 2B, Pm6 and Pm26, we believe it is a novel powdery mildew resistance gene and propose to designate this gene as Pm33.