Phytophthora root rot, caused by Phytophthora sojae, is a devastating soilborne disease of soybean (Glycine max). However, the epigenetic regulation of soybean responses to P. sojae remains incompletely understood. Here, using genetic, molecular and biochemical approaches, we characterized the functions of LIKE HETEROCHROMATIN PROTEIN 1 (GmLHP1) and its downstream regulatory network. We demonstrated that GmLHP1, as a reader of H3K27me3, negatively regulates soybean resistance to P. sojae. GmLHP1 binds to H3K27me3 peptides in vitro and colocalizes with H3K27me3 marks genome-wide in vivo. The integrated chromatin immunoprecipitation sequencing and RNA sequencing analysis identified the ethylene biosynthesis pathway gene 1-AMINO-CYCLOPROPANE-1-CARBOXYLATE SYNTHASE 18 (GmACS18) as being enriched for H3K27me3 and bound by GmLHP1, leading to its transcriptional downregulation. Notably, GmLHP1 associates with the GmACS18 promoter by directly binding to AATTAA motifs and recognizing H3K27me3 marks. Moreover, GmACS18 enhances defense against P. sojae by accumulating the ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC). Further analysis unveiled that recognition of H3K27me3 by GmLHP1 is essential for regulating soybean resistance to P. sojae through repressing GmACS18 transcription and decreasing ACC accumulation. Our findings reveal a novel epigenetic regulatory mechanism in which the H3K27me3 reader GmLHP1 blocks soybean resistance to P. sojae by repressing ethylene precursor ACC accumulation.

Phytophthora root rot, a devastating disease caused by Phytophthora sojae, poses a significant threat to worldwide soybean (Glycine max) production. Therefore, enhancing crop resistance to this pathogen is a major breeding objective. However, the signalling mechanisms underlying the response of soybean plants to P. sojae infection, and the networks and targets of key transcription factors TFs, are not yet fully understood. Here, we reveal the mechanisms and function of GmERF109, which differs in expression between soybean cultivars resistant and susceptible to P. sojae race 1 and encodes an AP2/ERF transcription factor. Molecular evaluation and disease resistance analysis show that GmERF109 is a nucleus-localized transcription factor that positively regulates soybean resistance to P. sojae. We also demonstrate that GmERF109 targets and activates the expression of GmG4DT-like, a gene whose role in the biosynthesis of the phytoalexin glyceollin was confirmed through overexpression and RNA interference (RNAi) analyses. GmG4DT-like also enhances P. sojae resistance. GmG4DT-like and GmERF109 greatly increased the content of the glyceollin I isomer. Overall, our results suggest that GmERF109 enhances glyceollin accumulation by positively regulating the expression of its target gene GmG4DT-like, thereby improving soybean resistance to P. sojae. These findings provide novel insights into soybean resistance to Phytophthora root rot and will be useful in efforts to create resistant soybean cultivars.

The transcription factor GmPEIN3 enhances resistance to Phytophthora sojae via ethylene-mediated antioxidant regulation and improves favorable agronomic traits in soybean. Phytophthora sojae is a devastating pathogen of soybean, and developing cultivars that combine high yield with strong disease resistance is a primary breeding objective. However, genes that coordinately regulate these two crucial traits have rarely been identified. In a previous study, using a combination of subtractive suppression hybridization (SSH) and cDNA microarray analysis on the highly resistant soybean variety ‘Suinong 10’, we identified a promising candidate, GmPEIN3 (Glycine max P. sojae-responsive EIN3), an EIN-type transcription factor. In this work, we confirmed that the expression of GmPEIN3 was potently induced by P. sojae infection in resistant soybean germplasm. Overexpression of GmPEIN3 in soybean resulted in enhanced resistance to P. sojae, while RNA-interference (RNAi) silencing led to increased susceptibility. Transcriptome analysis revealed that GmPEIN3 modulates plant hormone signal transduction and phenylpropanoid biosynthesis pathways. Consistently, ethylene (ET) levels, along with the activities and transcript levels of key antioxidant enzymes (SOD, POD, CAT, and GPX), were markedly higher in GmPEIN3-overexpressing (GmPEIN3-OE) transgenic soybean than in wild type (WT). Mechanistically, molecular assays demonstrated that GmPEIN3 directly binds to and transactivates the promoters of the ET biosynthesis gene GmACO3 and antioxidant-related genes GmSODB and GmPOD21, thereby promoting ET production and enhancing antioxidant defense capacity. Moreover, GmPEIN3-OE lines exhibited significant increases in effective pod number, seeds per plant, and 100-seed weight, whereas these traits were markedly reduced in RNAi lines. Taken together, these results suggest that GmPEIN3 plays a positive dual role in soybean, enhancing P. sojae resistance through the modulation of ethylene signaling and antioxidant defense systems, and simultaneously improving yield-related agronomic traits.

Protein phosphorylation and ubiquitination play central roles in signal transduction. SnRK1 is a key kinase that mediates plant responses to environmental cues. From a wild soybean cDNA library, we identified GsSRF2, which encodes a RING-domain E3 ligase that interacts with GsSnRK1. GsSRF2 is predominantly expressed in roots and responds dynamically to salt stress. BiFC, pull-down, and co-IP assays this interaction in the cytoplasm and at the plasma membrane. Biochemical analyses revealed that GsSnRK1 phosphorylates GsSRF2 at Thr514. GnSnRK1-mediated phosphorylation enhanced GsSRF2 ubiquitination and promoted its proteasomal degradation. Coexpression assays in soybean hairy roots demonstrated that the GsSnRK1-GsSRF2 module significantly improved salt tolerance, whereas the GsSnRK1-GsSRF2(T514A) and kinase-dead GsSnRK1(K49M)-GsSRF2 modules reduced salt resistance in composite plants. Together, these results indicate that GsSnRK1 positively regulates soybean salt tolerance by modulating GsSRF2 ligase activity and protein stability, providing valuable genetic resources for crop improvement.

Saline–alkali stress is becoming a major global issue due to environmental degradation, hindering plant growth and reducing both seed yield and quality of many crops, including soybean. Improving stress tolerance through genetic resources is crucial for sustainable production. In this study, overexpression of the Arabidopsis SRRM1L gene increased soybean (Glycine max) tolerance to saline–alkali stress by reducing reactive oxygen species and malondialdehyde accumulation and promoting antioxidant enzyme activities, whereas knockdown of GmSRRM1L1/2 genes reduced stress resistance and overexpression of GmSRRM1L1/2 increased it. These findings highlight that the AtSRRM1L and GmSRRM1L proteins are valuable genetic resources for breeding stress-resistant cultivars without yield penalty.

Soybean frogeye leaf spot (FLS) is a global fungal disease that adversely affects both the yield and quality of soybean. The available resistant loci and genes for FLS are limited, thereby constraining the molecular breeding of soybean for FLS resistance. In this study, a recombinant inbred lines (RIL) population (RIL3613), derived from the cross of Dongnong L13 and Heihe 36, was utilized to analyze the genetics of resistance and identify resistant loci. By combining the relative lesion area (RLA) data from each individual of RIL3613 collected across two environments with a high-density bin genetic map, a total of 19 quantitative trait loci (QTL) were identified, distributed across 9 chromosomes, with phenotypic variation explained (PVE) ranging from 1.12% to 18.93%. Notably, 8 QTL were consistently located in both environments, prompting a search for candidate genes within these stable QTL. Through parental sequence variation analysis, expression level determination, haplotype analysis, and gene function annotation, one gene (Glyma.15G245300) within qFLSm-15-1, which encodes cytochrome P450, was selected as a candidate gene. This study identified several novel loci and genes that may enhance molecular breeding efforts aimed at improving resistance to FLS in soybean.

Soybean (Glycine max) is a major economic and food crop whose yield is severely affected by frogeye leaf spot (FLS), caused by Cercospora sojina. Current knowledge of resistance genes remains insufficient for effective molecular breeding. In this study, a recombinant inbred line (RIL) population derived from a cross between the resistant parent, Henong 60 (H60), and the susceptible parent, Dongnong L13 (DN L13), was evaluated under field conditions in Acheng (AC) and Xiangyang (XY). Plants were artificially inoculated with physiological race 7 of C. sojina, and disease severity at the R3 growth stage was recorded. Genotyping using the SoySNP660K chip yielded 54,836 high-quality single-nucleotide polymorphism (SNP) markers. A genome-wide association study (GWAS) was performed using the 3VmrMLM model by integrating dual-environment phenotypic data, and four quantitative trait nucleotides (QTNs) significantly associated with resistance to FLS were identified on chromosomes 8 (1), 17 (1), and 20 (2). By the analysis of genomic annotation, functional enrichment, metabolic pathway analyses, haplotype-phenotype association and quantitative real-time PCR (qRT-PCR), Glyma.20G155700 and Glyma.17G070500 are intended to be candidate genes related to soybean resistance to race 7 of FLS. The findings of this study provide insights into the genetic mechanisms underlying resistance to FLS in soybean. The identified molecular markers and candidate genes may provide useful resources for marker-assisted breeding and the development of disease-resistant germplasm.

Wild soybean (Glycine soja) is a leguminous species known for its ability to thrive in challenging and barren environments. It has been reported that the nitrate transporters (NRTs) play critical roles for plants to survive in the nutrient-poor soils. However, the molecular mechanisms of GsNRTs in governing nitrogen (N) uptake remain largely elusive. In the present study, we identified a NRT2.4-like protein (GsNRT2.4a) as an interactor of GsSnRK1.1 kinase. Our biophysical and physiological analyses indicate that GsNRT2.4a functions as an active NRT, and GsSnRK1.1 kinase phosphorylates the Ser518 residue at the carboxyl region of GsNRT2.4a. Under N starvation conditions, the double mutant nrt2.1/nrt2.2 (2nrtm) and the quadruple mutant nrt2.1/nrt2.2/kin10/kin11 (2kinm/2nrtm) exhibited compromised growth of Arabidopsis. However, introduction of GsNRT2.4a or GsSnRK1.1/GsNRT2.4a genes into the mutants rescued their defective growth to different extent. Furthermore, we determined that GsSnRK1.1 plays a pivotal role in modulating GsNRT2.4a activity in planta by phosphorylating GsNRT2.4a at the Ser518 site, thereby collaboratively modulating plant growth under N starvation. Our findings suggest that GsNRT2.4a is essential for optimising nitrate uptake in plants, and it also elucidates a novel regulatory mechanism of GsSnRK1.1-GsNRT2.4a module for potential enhancement of nitrogen use efficiency (NUE) in plants.

The flowering time of soybean [Glycine max (L.) Merr.] is extremely sensitive to photoperiod, which importantly influences its yield potential and restricts the geographical range of soybean cultivars to specific latitudes. Molecular breeding to modulate flowering time and reduce sensitivity to day length is an effective approach to enhance the adaptability and productivity of soybean. Here, we characterized reproductive meristem 16a (GmREM16a), a member of the AP2/B3-like transcription factor family. The GmREM16a protein contains 2 B3 domains, and the expression of its encoding gene is responsive to photoperiod and circadian rhythm. The overexpression of GmREM16a in soybean accelerated flowering by regulating the expression of flowering-related genes. The GmREM16a protein was able to directly bind to the promoters of GmSOC1, GmFT2a, and GmFT5a and upregulate their expression. Yeast two-hybrid screening revealed that GmCSN5 interacts with GmREM16a. GmCSN5 is the fifth subunit of the COP9 signalosome (constitutively photomorphogenic signalosome, CSN) that regulates the activity of CULLIN-RING E3 ubiquitin ligases and regulates protein degradation. Protein degradation assays in vivo and in vitro showed that GmCSN5 promotes the degradation of GmREM16a protein via the ubiquitin-proteasome pathway. Taken together, these findings indicate that the transcription factor GmREM16a promotes flowering by regulating the expression of flowering-related genes. Additionally, GmCSN5 interacts with GmREM16a to regulate its stability in soybean. The GmREM16a-GmSCN5 module may represent a pathway involved in the regulation of flowering time in soybean and is a useful genetic resource for improving the adaptability of soybean through molecular breeding approaches.

Salineu2013alkali stress is becoming a major global issue due to environmental degradation, hindering plant growth and reducing both seed yield and quality of many crops, including soybean. Improving stress tolerance through genetic resources is crucial for sustainable production. In this study, overexpression of the Arabidopsis SRRM1L gene increased soybean (Glycine max) tolerance to salineu2013alkali stress by reducing reactive oxygen species and malondialdehyde accumulation and promoting antioxidant enzyme activities, whereas knockdown of GmSRRM1L1/2 genes reduced stress resistance and overexpression of GmSRRM1L1/2 increased it. These findings highlight that the AtSRRM1L and GmSRRM1L proteins are valuable genetic resources for breeding stress-resistant cultivars without yield penalty.

Transcriptomic analysis revealed that GmERF1 expression is induced by Phytophthora sojae and positively regulates soybean resistance to P. sojae via salicylic acid signal transduction pathway. Soybean (Glycine max) root rot caused by Phytophthora sojae is a major disease constraining the global soybean industry. Therefore, improving crop resistance to this pathogen remains a key objective in breeding efforts. However, the mechanisms by which soybeans respond to P. sojae infection, as well as the specific regulatory networks of key transcription factors (TFs), remain to be elucidated. Here, we report that Ethylene Response Factor 1 (GmERF1), encoding an AP2/ERF transcription factor, exhibits significant differences in expression between resistant and susceptible soybean cultivars. Molecular evaluation and disease resistance analysis show that GmERF1 could improve soybean resistance to P. sojae. Further transcriptomic analysis and quantitative analysis of salicylic acid (SA) signal transduction genes indicate that GmERF1 could positively regulate the expression of Non-expressor of Pathogenesis-Related genes 1 (GmNPR1), TGACG sequence-specific binding factor (GmTGA) and Pathogenesis-Related gene 1 (GmPR1). Taken together, these results suggest that GmERF1 positively regulates soybean resistance to P. sojae by enhancing SA signaling, providing novel insights into soybean resistance to Phytophthora root rot.

Soybean frogeye leaf spot (FLS) disease has been reported globally and is caused by the fungus Cercospora sojina, which affects the growth, seed yield, and quality of soybean. Among the 15 physiological microspecies of C. sojina soybean in China, Race 7 is one of the main pathogenic microspecies. A few genes are involved in resistance to FLS, and they cannot meet the need to design molecular breeding methods for disease resistance. In this study, a soybean recombinant inbred line (RIL3613) population and a germplasm resource (GP) population were planted at two sites, Acheng (AC) and Xiangyang (XY). Phenotypic data on the percentage of leaf area diseased (PLAD) in soybean leaves were obtained via image recognition technology after the inoculation of seven physiological species and full onset at the R3 stage. Quantitative trait loci (QTLs) and quantitative trait nucleotides (QTNs) were mapped via linkage analysis and genome-wide association studies (GWASs), respectively. The resistance genes of FLS were subsequently predicted in the linkage disequilibrium region of the collocated QTN. We identified 114 QTLs and 18 QTNs in the RIL3613 and GP populations, respectively. A total of 14 QTN loci were colocalized in the two populations, six of which presented high phenotypic contributions. Through haplotype–phenotype association analysis and expression quantification, three genes (Glyma.06G300100, Glyma.06G300600, and Glyma.13G172300) located near molecular markers AX-90524088 and AX-90437152 (QTNs) are associated with FLS Chinese Race 7, identifying them as potential candidate resistance genes. These results provide a theoretical basis for the genetic mining of soybean antigray spot No. 7 physiological species. These findings also provide a theoretical basis for understanding the genetic mechanism underlying FLS resistance in soybeans.

Phytophthora root and stem rot is a destructive soybean disease worldwide, and thus improving soybean resistance to P. sojae is a major breeding target. However, the complex regulatory networks governing host defense remain unclear. Our previous study showed that GmWRKY40 positively regulates resistance of soybean to P. sojae. Here, to explore its molecular mechanism, we found that GmWRKY40 is induced by P. sojae in resistant cultivars and that the protein localizes in nucleus. RNA-seq and metabolomic analyses revealed that GmWRKY40 modulates the jasmonate (JA) signaling pathway. We then found that GmWRKY40 directly suppresses the key JA repressor GmJAZ1 by binding to the promoter. This leads to higher endogenous JA levels, and the overall state of enhanced resistance is also characterized by elevated SOD and POD antioxidant enzyme activity. Furthermore, we demonstrated that GmWRKY40 interacts with GmWRKY36, a transcription factor identified as a negative regulator of P. sojae infection in this research. Taken together, our study delineates a novel regulatory module where GmWRKY40 enhances resistance to P. sojae through a dual mechanism: activating the JA pathway by repressing its suppressor GmJAZ1, and engaging in a potentially antagonistic interaction with the negative regulator GmWRKY36, ultimately enhancing soybean resistance to P. sojae.

Phytophthora root and stem rot of soybean (Glycine max), caused by the oomycete Phytophthora sojae, is an extremely destructive disease worldwide. In this study, we identified GmEIL1, which encodes an ethylene-insensitive3 (EIN3) transcription factor. GmEIL1 was significantly induced following P. sojae infection of soybean plants. Compared to wild-type soybean plants, transgenic soybean plants overexpressing GmEIL1 showed enhanced resistance to P. sojae and GmEIL1-silenced RNA-interference lines showed more severe symptoms when infected with P. sojae. We screened for target genes of GmEIL1 and confirmed that GmEIL1 bound directly to the GmERF113 promoter and regulated GmERF113 expression. Moreover, GmEIL1 positively regulated the expression of the pathogenesis-related gene GmPR1. The GmEIL1-regulated defence response to P. sojae involved both ethylene biosynthesis and the ethylene signalling pathway. These findings suggest that the GmEIL1-GmERF113 module plays an important role in P. sojae resistance via the ethylene signalling pathway.

Phytophthora root rot is a devastating disease of soybean caused by Phytophthora sojae. However, the resistance mechanism is not yet clear. Our previous studies have shown that GmAP2 enhances sensitivity to P. sojae in soybean, and GmMYB78 is downregulated in the transcriptome analysis of GmAP2-overexpressing transgenic hairy roots. Here, GmMYB78 was significantly induced by P. sojae in susceptible soybean, and the overexpressing of GmMYB78 enhanced sensitivity to the pathogen, while silencing GmMYB78 enhances resistance to P. sojae, indicating that GmMYB78 is a negative regulator of P. sojae. Moreover, the jasmonic acid (JA) content and JA synthesis gene GmAOS1 was highly upregulated in GmMYB78-silencing roots and highly downregulated in overexpressing ones, suggesting that GmMYB78 could respond to P. sojae through the JA signaling pathway. Furthermore, the expression of several pathogenesis-related genes was significantly lower in GmMYB78-overexpressing roots and higher in GmMYB78-silencing ones. Additionally, we screened and identified the upstream regulator GmbHLH122 and downstream target gene GmbZIP25 of GmMYB78. GmbHLH122 was highly induced by P. sojae and could inhibit GmMYB78 expression in resistant soybean, and GmMYB78 was highly expressed to activate downstream target gene GmbZIP25 transcription in susceptible soybean. In conclusion, our data reveal that GmMYB78 triggers soybean sensitivity to P. sojae by inhibiting the JA signaling pathway and the expression of pathogenesis-related genes or through the effects of the GmbHLH122-GmMYB78-GmbZIP25 cascade pathway.

Phytophthora root and stem rot caused by Phytophthora sojae Kaufmann and Gerdemann is a soil-borne disease severely affecting soybean production worldwide. Losses caused by P. sojae can be controlled by both major genes and quantitative trait locus. Here, we tested 112 short-season soybean cultivars from Northeast China for resistance to P. sojae. A total of 58 germplasms were resistant to 7–11 P. sojae strains. Among these, Mengdou 28 and Kejiao 10-262 may harbor either Rps3a or multiple Rps genes conferring resistance to P. sojae. The remaining 110 germplasms produced 91 reaction types and may contain new resistance genes or gene combinations. Partial resistance evaluation using the inoculum layer method revealed that 34 soybean germplasms had high partial resistance, with a mean disease index lower than 30. Combining the results of resistance and partial resistance analyses, we identified 35 excellent germplasm resources as potential elite materials for resistance and tolerance in future breeding programs. In addition, we compared the radicle inoculation method with the inoculum layer method to screen for partial resistance to P. sojae. Our results demonstrate that the radicle inoculation method could potentially replace the inoculum layer method to identify partial resistance against P. sojae, and further verification with larger samples is required in the future.

Phytophthora root rot is a destructive soybean disease worldwide, which is caused by the oomycete pathogen Phytophthora sojae (P. sojae). Wall-associated protein kinase (WAK) genes, a family of the receptor-like protein kinase (RLK) genes, play important roles in the plant signaling pathways that regulate stress responses and pathogen resistance. In our study, we found a putative Glycine max wall-associated protein kinase, GmWAK1, which we identified by soybean GmLHP1 RNA-sequencing. The expression of GmWAK1 was significantly increased by P. sojae and salicylic acid (SA). Overexpression of GmWAK1 in soybean significantly improved resistance to P. sojae, and the levels of phenylalanine ammonia-lyase (PAL), SA, and SA-biosynthesis-related genes were markedly higher than in the wild-type (WT) soybean. The activities of enzymatic superoxide dismutase (SOD) and peroxidase (POD) antioxidants in GmWAK1-overexpressing (OE) plants were significantly higher than those in in WT plants treated with P. sojae; reactive oxygen species (ROS) and hydrogen peroxide (H2O2) accumulation was considerably lower in GmWAK1-OE after P. sojae infection. GmWAK1 interacted with annexin-like protein RJ, GmANNRJ4, which improved resistance to P. sojae and increased intracellular free-calcium accumulation. In GmANNRJ4-OE transgenic soybean, the calmodulin-dependent kinase gene GmMPK6 and several pathogenesis-related (PR) genes were constitutively activated. Collectively, these results indicated that GmWAK1 interacts with GmANNRJ4, and GmWAK1 plays a positive role in soybean resistance to P. sojae via a process that might be dependent on SA and involved in alleviating damage caused by oxidative stress.

Phytophthora root and stem rot is a worldwide soybean (Glycine max) disease caused by the soil-borne pathogen Phytophthora sojae. This disease is devastating to soybean production, so improvement of resistance to P. sojae is a major target in soybean breeding. Mitogen-activated protein kinase (MAPK) cascades are important signaling modules that convert environmental stimuli into cellular responses. Compared with extensive studies in Arabidopsis, the molecular mechanism of MAPK cascades in soybean disease resistance is barely elucidated. In this work, we found that the gene expression of mitogen-activated protein kinase 6 (GmMPK6) was potently induced by P. sojae infection in the disease-resistant soybean cultivar 'Suinong 10'. Overexpression of GmMPK6 in soybean resulted in enhanced resistance to P. sojae and silencing of GmMPK6 led to the opposite phenotype. In our attempt to dissect the role of GmMPK6 in soybean resistance to phytophthora disease, we found that MAPK kinase 4 (GmMKK4) and the ERF transcription factor GmERF113 physically interact with GmMPK6, and we determined that GmMKK4 could phosphorylate and activate GmMPK6, which could subsequently phosphorylate GmERF113 upon P. sojae infection, suggesting that P. sojae can stimulate the GmMKK4-GmMPK6-GmERF113 signaling pathway in soybean. Moreover, phosphorylation of GmERF113 by the GmMKK4-GmMPK6 module promoted GmERF113 stability, nuclear localization and transcriptional activity, which significantly enhanced expression of the defense-related genes GmPR1 and GmPR10-1 and hence improved disease resistance of the transgenic soybean seedlings. In all, our data reveal that the GmMKK4-GmMPK6-GmERF113 cascade triggers resistance to P. sojae in soybean and shed light on functions of MAPK kinases in plant disease resistance.

The objective of this study was to determine if genotypes with differing globulin subunit compositions affect the hypocholesterolemic effect (HCE) of soy protein isolates (SPIs). Six SPIs (300 mg/kg/day), which differed in the 11S/7S globulin subunit composition, and fenofibrate (FF) (30 mg/kg/day), a hypocholesterolemic drug, were administered by gavage for 28 days to hypercholesterolemic model rats (HMRs). Blood samples were collected to measure serum lipid parameters. Hepatic histopathologic and lipid biochemical data were collected, and the expression of cholesterol metabolism-related key genes was analyzed. Our results demonstrated that soybeans differing in genotype generate SPIs with marked different HCEs, and the mechanism underlying the various HCEs of SPIs is associated with differential expression of hepatic cholesterol metabolism-related key genes in HMRs. 7S(α′+α)-Null genotype provided a greater effect on increasing HDL-C level, and daily ingestion of SPI-2 (null α′, α) might significantly contribute to increase HDL-C level in HMRs.

大豆是关系国计民生的重要基础性、战略性物资,在国际农产品贸易领域具有举足轻重的地位.然而大豆蛋白也是人类食品八大致敏原之一,大豆中含有的抗原蛋白会导致人和动物发生过敏反应,如何减少或彻底清除大豆过敏蛋白,保证大豆蛋白的安全、广泛应用,是大豆蛋白品质改良的重要科学问题之一.