Citric acid is an important contributor to fruit flavor.The extremely significant differences in citric acid levels are observed among citrus species and varieties.The molecular basis of citric acid accumulation remai...Citric acid is an important contributor to fruit flavor.The extremely significant differences in citric acid levels are observed among citrus species and varieties.The molecular basis of citric acid accumulation remains largely unknown on the inter-species level.Here,we performed transcriptome analysis of five pairs of acidic and acidless variety fruits from kumquat(Citrus crassifolia),lemon(C.limon),pummelo(C.maxima),mandarin(C.reticulata),and sweet orange(C.sinensis)to investigate the common and specific genes related to citric acid accumulation in these citrus species.Transcript profiles of the citrate metabolism genes revealed that the mechanism of citric acid accumulation in kumquat differed from that in the other four species.The comparative analysis and weighted gene co-expression network analysis identified 61 candidate genes from lemon,pummelo,mandarin,and sweet orange.Vacuolar acidification regulated by CitPH4-CitAN1-CitPH5was a common mechanism underlying citric acid accumulation in these four species.In addition,gene network analysis indicated that CitPH4 was a central regulator,exhibiting a strong correlation with the genes involved in vacuolar trafficking and potassium(K^(+))transport.The co-expression and functional enrichment analyses showed that active sugar metabolism and increased citrate synthesis were mainly responsible for the accumulation of citric acid in kumquat.Twenty-four transcription factors were identified as candidate regulators,of which CitbHLH28 was found to regulate acidity level via transactivating CWINV2 and PK3 expressions.Overall,this study provides an insight into the mechanism of citric acid accumulation in citrus fruit and provides useful references for fruit quality improvement through acidity control in different citrus species.展开更多
目的:观察乳酸杆菌对蒙古沙土鼠H pylori感染性胃炎的治疗作用,探讨乳酸杆菌防治H pylori感染的作用机制.方法:通过接种H pylori,建立蒙古沙土鼠H p y l o r i感染性胃炎动物模型,将造模成功的32只蒙古沙土鼠随机分为4组,每组8只.第1组...目的:观察乳酸杆菌对蒙古沙土鼠H pylori感染性胃炎的治疗作用,探讨乳酸杆菌防治H pylori感染的作用机制.方法:通过接种H pylori,建立蒙古沙土鼠H p y l o r i感染性胃炎动物模型,将造模成功的32只蒙古沙土鼠随机分为4组,每组8只.第1组(抗生素加质子泵抑制剂干预治疗组)、第2组(乳酸杆菌治疗组)、第3组(乳酸杆菌加质子泵抑制剂治疗组)、第4组(生理盐水对照组),用相应干扰剂分别连续灌胃治疗10d.另8只正常蒙古沙土鼠为第5组(空白对照组).最后1次灌胃4wk后处死沙鼠,HE染色判断鼠胃黏膜组织学损伤,并用快速尿素酶试验、Giemsa染色和细菌培养进行H pylori的检测,免疫组化检测胃黏膜中IL-6、COX-2、和TNF-α蛋白的表达.结果:第1组、第2组和第3组之间蒙古沙土鼠的H pylori根除率无显著差异,但均比第4组的根除率低,之间差异有显著性(87.5%,75%,75%vs100%,均P<0.05).第1组、第2组和第3组蒙古沙土鼠的胃体、胃窦和十二指肠各部位组织胃黏膜慢性炎症评分与第4组相比显著下降(胃体:1.8±0.54,2.0±0.48,1.9±0.50vs4.2±1.06,均P<0.05;胃窦:1.5±0.27,1.4±0.33,1.7±0.46vs4.6±0.74,均P<0.05;十二指肠:1.4±0.41,1.7±0.29,1.6±0.52vs4.1±0.83,均P<0.05).第1组、第2组和第3组蒙古沙土鼠三种炎症因子表达与第4组相比显著下降(COX-2:3.57±0.32,3.89±0.51,2.95±0.76vs6.79±1.68,均P<0.05;IL-6:2.42±0.60,2.28±0.71,1.93±0.52vs5.61±0.28,均P<0.05;TNF-α:3.30±0.52,3.65±0.35,2.84±0.20vs6.76±1.63,均P<0.05).结论:乳酸杆菌治疗蒙古沙鼠H pylori感染性胃炎模型的疗效与PPI加抗生素三联疗法相当;并可显著降低沙鼠胃黏膜的COX-2、IL-6、TNF-α的表达.展开更多
基金financially supported by the National Natural Science Foundation of China(Grant No.31925034)the National Key Research and Development Program of China(Grant No.2022YFF1003100)+1 种基金the Foundation of Hubei Hongshan Laboratory(Grant No.2021hszd016)Key project of Hubei provincial Natural Science Foundation(Grant No.2021CFA017)。
文摘Citric acid is an important contributor to fruit flavor.The extremely significant differences in citric acid levels are observed among citrus species and varieties.The molecular basis of citric acid accumulation remains largely unknown on the inter-species level.Here,we performed transcriptome analysis of five pairs of acidic and acidless variety fruits from kumquat(Citrus crassifolia),lemon(C.limon),pummelo(C.maxima),mandarin(C.reticulata),and sweet orange(C.sinensis)to investigate the common and specific genes related to citric acid accumulation in these citrus species.Transcript profiles of the citrate metabolism genes revealed that the mechanism of citric acid accumulation in kumquat differed from that in the other four species.The comparative analysis and weighted gene co-expression network analysis identified 61 candidate genes from lemon,pummelo,mandarin,and sweet orange.Vacuolar acidification regulated by CitPH4-CitAN1-CitPH5was a common mechanism underlying citric acid accumulation in these four species.In addition,gene network analysis indicated that CitPH4 was a central regulator,exhibiting a strong correlation with the genes involved in vacuolar trafficking and potassium(K^(+))transport.The co-expression and functional enrichment analyses showed that active sugar metabolism and increased citrate synthesis were mainly responsible for the accumulation of citric acid in kumquat.Twenty-four transcription factors were identified as candidate regulators,of which CitbHLH28 was found to regulate acidity level via transactivating CWINV2 and PK3 expressions.Overall,this study provides an insight into the mechanism of citric acid accumulation in citrus fruit and provides useful references for fruit quality improvement through acidity control in different citrus species.
文摘目的:观察乳酸杆菌对蒙古沙土鼠H pylori感染性胃炎的治疗作用,探讨乳酸杆菌防治H pylori感染的作用机制.方法:通过接种H pylori,建立蒙古沙土鼠H p y l o r i感染性胃炎动物模型,将造模成功的32只蒙古沙土鼠随机分为4组,每组8只.第1组(抗生素加质子泵抑制剂干预治疗组)、第2组(乳酸杆菌治疗组)、第3组(乳酸杆菌加质子泵抑制剂治疗组)、第4组(生理盐水对照组),用相应干扰剂分别连续灌胃治疗10d.另8只正常蒙古沙土鼠为第5组(空白对照组).最后1次灌胃4wk后处死沙鼠,HE染色判断鼠胃黏膜组织学损伤,并用快速尿素酶试验、Giemsa染色和细菌培养进行H pylori的检测,免疫组化检测胃黏膜中IL-6、COX-2、和TNF-α蛋白的表达.结果:第1组、第2组和第3组之间蒙古沙土鼠的H pylori根除率无显著差异,但均比第4组的根除率低,之间差异有显著性(87.5%,75%,75%vs100%,均P<0.05).第1组、第2组和第3组蒙古沙土鼠的胃体、胃窦和十二指肠各部位组织胃黏膜慢性炎症评分与第4组相比显著下降(胃体:1.8±0.54,2.0±0.48,1.9±0.50vs4.2±1.06,均P<0.05;胃窦:1.5±0.27,1.4±0.33,1.7±0.46vs4.6±0.74,均P<0.05;十二指肠:1.4±0.41,1.7±0.29,1.6±0.52vs4.1±0.83,均P<0.05).第1组、第2组和第3组蒙古沙土鼠三种炎症因子表达与第4组相比显著下降(COX-2:3.57±0.32,3.89±0.51,2.95±0.76vs6.79±1.68,均P<0.05;IL-6:2.42±0.60,2.28±0.71,1.93±0.52vs5.61±0.28,均P<0.05;TNF-α:3.30±0.52,3.65±0.35,2.84±0.20vs6.76±1.63,均P<0.05).结论:乳酸杆菌治疗蒙古沙鼠H pylori感染性胃炎模型的疗效与PPI加抗生素三联疗法相当;并可显著降低沙鼠胃黏膜的COX-2、IL-6、TNF-α的表达.
