细菌感染/ 定植诱导慢性阻塞性肺疾病患者痰β- 防御素2 表达

目的:初步探讨下呼吸道细菌感染/定植对慢性阻塞性肺疾病(COPD)患者痰β-防御素2(BD-2)表达水平的影响。方法:36例戒烟COPD患者和30名不吸烟/戒烟对照人员纳入研究。在COPD患者的急性加重期和稳定期分别采集自然痰进行普通细菌培养(简称痰培养),并行细胞分类计数和BD-2浓度测定;采集对照人员诱导痰行细胞分类计数和BD-2浓度测定以资对照。结果:COPD患者急性加重期和稳定期痰培养阳性比例分别为30/36和14/36。COPD患者痰细胞总数和中性粒细胞比例、淋巴细胞比例高于对照组而巨噬细胞比例低于对照组;痰菌阳性和痰菌阴性的急性加重期COPD患者痰细胞总数、巨噬细胞比例、中性粒细胞比例分别为(6.0±0.9)×106/g、(23.6±3.9)%、(66.0±5.9)%和(3.1±0.5)×106/g、(34.3±4.3)%、(55.7±4.4)%,痰菌阳性和痰菌阴性的稳定期COPD患者痰细胞总数、巨噬细胞比例、中性粒细胞比例、淋巴细胞比例分别为(4.4±0.8)×106/g、(28.6±6.4)%、(64.0±7.2)%和(3.0±0.5)×106/g、(41.4±5.7)%、(45.4±5.1)%。COPD患者稳定期痰BD-2浓度[(211±98)ng/L]低于急性加重期[(300±83)ng/L]而高于对照组[(127±41)ng/L];痰菌阳性稳定期COPD患者痰BD-2浓度高于对照组而与急性加重期无统计学差异;痰菌阴性稳定期COPD患者痰BD-2浓度低于急性加重期而与对照组无统计学差异。结论:下呼吸道细菌感染/定植是COPD患者痰BD-2表达升高的重要诱导因素,也是COPD患者急性加重发作的重要原因。     

慢性阻塞性肺疾病大鼠模型中痩素及白介素-8 的表达分析

目的:观察COPD大鼠模型中瘦素(leptin)、白细胞介素8(IL-8)的表达情况,分析其相关性,探讨leptin在COPD发生发展中的作用及意义.方法:36只雄性SD大鼠随机分为①健康对照组;②COPD模型1组:分别于第(1、14)d经气管内注入内毒素200ug,熏5％香烟(第1、14d除外),2h/d,共4周;③COPD模型2组:单纯熏5％香烟2h/d,共12周.观察肺组织病理变化,免疫组化法测定leptin、IL-8在支气管肺组织的表达情况,放免法测定血清leptin及IL-8浓度.结果:细胞因子leptin及炎性因子IL-8在支气管肺组织阳性表达.LPS联合熏烟诱导COPD1组支气管肺组织中leptin(52.67±04.72)和IL-8(59.56± 3.94)表达较单纯熏烟诱导COPD2组leptin(38.89± 2.57)和IL-8(55.22± 3.42)表达明显升高,P＜0.05,两组COPD大鼠模型支气管肺组织中leptin及IL-8表达较正常对照组leptin( 1690± 1.52)和IL-8 (28.00± 4.24)表达均明显增高,P＜0.05,COPD1组血清中leptin(3.26± 0.95)ng/mL和IL-8( 107.51±13.38 )pg/mL-较COPD2组中leptin(2.42± 0.69 )ng/mL和IL-8((94.07± 11.20)pg/mL明显增高,P＜0.05,两组COPD大鼠模型血清中leptin及IL-8浓度较正常对照组leptin(0.95±0.56)ng/mL和IL-8( 39.48± 6.35 )pg/mL浓度显著升高,P＜0.05.血清中Leptin与IL-8表达水平呈显著正相关(r值分别为0.72 0.67 0.84均P＜0.05).经过q检验,两两之间比较均有统计学意义.结论:leptin和IL-8均参与COPD炎症反应过程,并且具有相关性,LPS促进二者的表达.     

乙型肝炎肝硬化患者血清sICAM-1、IL-6、IL-18及TNF-α水平的表达及临床意义

目的:检测乙型肝炎肝硬化患者血清可溶性细胞间黏附分子-1(s ICAM-1)、白细胞介素-6(IL-6)、白细胞介素-18(IL-18)及肿瘤坏死因子-α(TNF-α)水平,并探讨其临床意义。方法:选取2017年1月至2019年6月我院收治的乙型肝炎肝硬化患者82例作为研究组,同期健康体检者80例作为对照组。比较研究组和对照组及不同Child-Pugh分级乙型肝炎肝硬化患者血清s ICAM-1、IL-6、IL-18、TNF-α、肝功能指标血浆谷丙氨酸氨基转移酶(ALT)、白蛋白(ALB)水平,并分析各指标之间的相关性。结果:研究组血清s ICAM-1、IL-6、IL-18、TNF-α和血浆ALT水平分别为(820.78±85.73)ng/mL、(41.71±13.24)ng/mL、(119.85±45.56)pg/mL、(52.23±22.24)ng/L、(155.20±56.27)U/L,显著高于对照组的(175.51±41.82)ng/mL、(6.67±2.23)ng/mL、(68.71±23.24)pg/mL、(5.65±1.28)ng/L、(15.65±5.23)U/L(P0.05),血浆ALB水平显著低于对照组[(27.69±4.32)g/L vs(45.16±5.65)g/L](P0.05)。随Child-Pugh分级的升高,乙型肝炎肝硬化患者血清s ICAM-1、IL-6、IL-18、TNF-α和血浆ALT水平逐渐升高,血浆ALB水平逐渐降低(P0.05)。乙型肝炎肝硬化患者血清s ICAM-1、IL-6、IL-18及TNF-α水平与血浆ALT水平呈正相关(P均0.05),与血浆ALB水平呈负相关(P均0.05),乙型肝炎肝硬化患者血清s ICAM-1与IL-6、IL-18及TNF-α呈正相关(P均0.05)。结论:乙型肝炎肝硬化患者血清s ICAM-1、IL-6、IL-18、TNF-α水平异常升高,与Child-Pugh分级和肝功能有关,检测血清s ICAM-1、IL-6、IL-18、TNF-α可能为乙型肝炎肝硬化的诊断和病情严重程度的判断提供依据。     

miR-125b在急性加重期慢性阻塞性肺疾病患者血浆中的表达及与肺功能和炎症细胞因子的关系

目的:探讨微小RNA-125b(miR-125b)在急性加重期慢性阻塞性肺疾病(COPD)患者血浆中的表达及其与肺功能、炎症细胞因子的关系。方法:选择2016年11月至2019年1月应急总医院收治的69例急性加重期COPD患者作为急性加重组,并于同期随机选取58例稳定期COPD患者作为稳定组和50例健康体检者作为对照组。采用实时荧光定量PCR法检测各组血浆miR-125b表达水平;采用肺功能检测仪测定肺功能,包括用力肺活量(FVC)、第1秒用力呼气量(FEV_1)、FEV_1/FVC;采用酶联免疫吸附法测定血清炎症细胞因子,包括白细胞介素-6(IL-6)、白细胞介素-8(IL-8)、高敏C反应蛋白(hs-CRP)、肿瘤坏死因子-α(TNF-α)。结果:急性加重组血浆miR-125b表达水平高于稳定组和对照组,差异有统计学意义(P0.05)。急性加重组、稳定组肺功能指标FVC、FEV_1、FEV_1/FVC低于对照组,且急性加重组低于稳定组,差异有统计学意义(P0.05)。急性加重组、稳定组血清炎症细胞因子IL-6、IL-8、hs-CRP、TNF-α水平高于对照组,且急性加重组高于稳定组,差异有统计学意义(P0.05)。Pearson相关分析结果显示,急性加重期COPD患者血浆miR-125表达水平与FVC、FEV_1、FEV_1/FVC呈负相关(P0.05),与IL-6、IL-8、hs-CRP、TNF-α呈正相关(P0.05)。结论:miR-125b在急性加重期COPD患者血浆中异常表达,并与肺功能及炎症细胞因子密切相关,可作为临床辅助诊断及评估患者病情严重程度的参考指标。     

IL-12，IFN-γ，EPO及铁蛋白在急性白血病患者血清中的表达及临床意义

目的:研究急性白血病患者血清白介素-12(IL-12)、γ干扰素(IFN-γ)、促红细胞生成素(EPO)、铁蛋白的表达及临床意义。方法:选取2015年8月至2016年7月我院收治的76例急性白血病患者视为观察组,初治组31例,缓解组25例,复发组20例;另选择同期在我院进行健康体检的76例视为对照组。比较急性白血病患者、健康人群及不同疾病阶段的血清IL-12、IFN-γ、EPO、铁蛋白水平。结果:观察组的IL-12、IFN-γ水平显著低于对照组,EPO、铁蛋白水平显著高于对照组,差异均有统计学意义(P0.05)。初治组、复发组的血清IL-12、IFN-γ显著低于缓解组[(84.21±5.43)pg/mL、(98.7±7.98)pg/mL比(112.43±10.21)pg/mL,(38.54±3.56)pg/mL、(49.87±4.02)pg/mL比(108.32±8.43)pg/mL](P0.05),EPO、铁蛋白水平显著高于缓解组[(402.32±42.31)mIU/mL、(321.58±30.21)mIU/mL比(98.21±9.45)mIU/mL,(653.21±54.24)ng/mL、(512.87±43.45)ng/mL比(342.15±25.12)ng/mL](P0.05)。结论:急性白血病患者血清IL-12、IFN-γ水平较低,EPO、铁蛋白的表达较高,可通过监测上述指标变化评估病情及预后。     

细菌感染/定植诱导慢性阻塞性肺疾病患者痰β-防御素2表达

目的：初步探讨下呼吸道细菌感染/定植对慢性阻塞性肺疾病（COPD）患者痰β-防御素2（BD-2）表达水平的影响。方法：36例戒烟COPD患者和30名不吸烟/戒烟对照人员纳入研究。在COPD患者的急性加重期和稳定期分别采集自然痰进行普通细菌培养（简称痰培养）,并行细胞分类计数和BD-2浓度测定;采集对照人员诱导痰行细胞分类计数和BD-2浓度测定以资对照。结果：COPD患者急性加重期和稳定期痰培养阳性比例分别为30/36和14/36。COPD患者痰细胞总数和中性粒细胞比例、淋巴细胞比例高于对照组而巨噬细胞比例低于对照组;痰菌阳性和痰菌阴性的急性加重期COPD患者痰细胞总数、巨噬细胞比例、中性粒细胞比例分别为（6.0±0.9）×106/g、（23.6±3.9）%、（66.0±5.9）%和（3.1±0.5）×106/g、（34.3±4.3）%、（55.7±4.4）%,痰菌阳性和痰菌阴性的稳定期COPD患者痰细胞总数、巨噬细胞比例、中性粒细胞比例、淋巴细胞比例分别为（4.4±0.8）×106/g、（28.6±6.4）%、（64.0±7.2）%和（3.0±0.5）×106/g、（41.4±5.7）%、（45.4±5.1）%。COPD患者稳定期痰BD-2浓度[（211±98）ng/L]低于急性加重期[（300±83）ng/L]而高于对照组[（127±41）ng/L];痰菌阳性稳定期COPD患者痰BD-2浓度高于对照组而与急性加重期无统计学差异;痰菌阴性稳定期COPD患者痰BD-2浓度低于急性加重期而与对照组无统计学差异。结论：下呼吸道细菌感染/定植是COPD患者痰BD-2表达升高的重要诱导因素,也是COPD患者急性加重发作的重要原因。     

Th17及Th1相关细胞因子与支气管哮喘的关系研究

目的:分析外周血Th17、Th1及相关细胞因子表达水平和支气管哮喘(bronchial asthma,BA)发生、发展的相关性研究。方法:回顾选取我院收治的BA病例57份,称作BA组,另选取呼吸系统正常的病例55例为对照组,检测两组入选者的外周血IL-2、TNF-α、Th17、IL-6、Th1指标表达差异,并进行多因素回归分析。结果:BA组Th17(0.62±1.67)%、Th1(1.45±0.48)%及Th1/Th17(2.33±1.28)均显著低于对照组(P均0.05);BA组TNF-α(27.46±8.12)pg/mL、IL-6(11.69±2.14)pg/mL表达量显著高于对照组,IL-2(2.58±3.89)pg/mL、IFN-γ(3.74±6.15)pg/mL含量均显著低于对照组(P均0.05);经Logistic回归分析,TNF-α、IL-6、IFN-γ、Th1/Th17、IL-2均和BA有密切相关性(P均0.05)。结论:IL-2、IFN-γ、Th1/Th17、TNF-α、IL-6表达水平均与BA有密切关联,可能是参与BA发病的主要原因,及早进行Th17、Th1及相关细胞因子检查有助于明确病情。     

IL-17在COPD稳定期、急性加重期患者中的表达及其意义

目的:分析慢性阻塞性肺疾病稳定期、急性加重期(COPD、AECOPD)患者血清白细胞介素17(IL-17)表达水平的差异,探讨血清IL-17在评价COPD患者病情严重程度及预后中的价值。方法:收集符合纳入标准的COPD、AECOPD患者、正常对照组(健康体检者)各50例。取各组血清标本测表达浓度,比较各组血清IL-17水平,并进行相关性分析。结论:COPD、AECOPD患者血清中IL-17明显高于正常对照组,差异有统计学意义。检测血清IL-17表达水平有助于评估COPD患者的病情严重程度和预后。     

甲氨蝶呤联合艾得辛可降低RA患者血清中IL-37及PD-1的水平

分析甲氨蝶呤联合艾得辛治疗对类风湿关节炎患者血清IL-37及PD-1水平的影响。选择2015年4月至2017年3月本院接诊的100例类风湿关节炎患者作为研究对象,按随机数字表法分组,每组50例,观察组患者采用甲氨蝶呤与艾得辛联合治疗,对照组患者单独采用甲氨蝶呤治疗,比较两组患者血清中细胞因子IL-6、IL-18和IL-18BP的表达,探讨IL-37、PD-1的临床意义。观察组患者的血清IL-18(63.23±7.89) pg/mL、IL-6 (3.25±0.98) pg/mL、IL-18BP (210.56±24.51) pg/mL表达水平显著低于对照组患者的血清IL-18 (140.67±18.65) pg/m L、IL-6 (8.27±1.23) pg/mL、IL-18BP (308.89±30.67) pg/mL表达水平;观察组患者的血清IL-37 (23.65±4.28) pg/m L及PD-1 (19.58±3.78) ng/mL表达水平显著低于对照组患者的血清IL-37 (58.98±5.29) pg/mL及PD-1 (36.72±4.62) ng/mL表达水平,差异具有统计学意义(p0.05),相关性分析发现,血清IL-37与细胞因子IL-18、IL-6和IL-18BP均呈正相关;但是PD-1仅与细胞因子IL-6呈正相关,按照RA评分标准,患者血清中IL-37与诊断评分呈正相关,PD-1与诊断评分呈正相关。甲氨蝶呤联合艾得辛治疗类风湿关节炎具有较为明确的疗效,能够短期内控制RA患者疾病的发展,临床的表现稳定,有效降低患者的血清IL-18、IL-6、IL-18BP以及IL-37、PD-1的表达水平,对患者的积极意义较大,可在临床的治疗中推广应用。     

甲状腺全切术治疗分化型甲状腺癌的疗效观察及临床研究探讨

目的:研究甲状腺全切术治疗分化型甲状腺癌的疗效观察及临床研究探讨。方法:收集2014年3月至2015年3月我院收治的90例分化型甲状腺癌患者,按抽签法分为实验组和对照组,每组45例。对照组采用次全切除术治疗,实验组采用甲状腺全切术治疗。观察两组患者的治疗疗效、手术时间、术中出血量、住院时间、复发率、治疗前后血清TNF-α、IL-6、Gal-3、VEGF水平及并发症的发生情况。结果:治疗后,实验组总有效率显著高于对照组[93.33%(42/45)vs68.89%(31/45)](P0.05)。两组住院时间比较差异无统计学意义(P0.05),实验组手术时间、术中出血量、复发率均显著低于对照组[(70.36±12.72)min vs(109.75±15.37)min,(50.28±10.64)mL vs(91.62±13.50)mL,2.22%(1/45)vs15.56%(7/45)](P0.05);治疗后血清TNF-α、IL-6、Gal-3、VEGF水平均显著低于对照组[(506.30±78.23)pg/mL vs(621.25±83.54)pg/mL,(73.29±10.32)pg/mL vs(102.58±12.49)pg/mL,(3.40±0.80)ng/mL vs(4.82±0.81)ng/mL,(16.21±4.02)pg/mL vs(20.75±5.23)pg/mL](P0.05)。实验组和对照组并发症总发生率分别为15.56%、6.66%,两组比较差异无统计学意义(P0.05)。结论:甲状腺全切术治疗分化型甲状腺癌的疗效优于次全切除术治疗,可彻底清除病灶,降低复发率,可能与有效降低患者血清TNF-α、IL-6、Gal-3、VEGF水平有关,但其并发症较多,对于低危或术后无需放射治疗的患者可采用次全切除术治疗,应慎重选择手术方式。     

LINE-1编码蛋白L1-ORF1的原核表达纯化和多克隆抗体制备

目的: 制备具有肿瘤组织特异性表达的L1-ORF1蛋白多克隆抗体并进行初步应用研究。方法:采取基因工程表达方法制备L1-ORF1蛋白,免疫家兔制备多克隆抗体,间接ELISA检测抗体效价,Western blot和细胞免疫荧光方法检测抗体特异性,免疫检测验证其识别肿瘤细胞内L1-ORF1蛋白的特异性。结果:制备的抗L1-ORF1蛋白多克隆抗体具有很高的敏感性与特异性,免疫学检测表明该抗体不仅能检测出正常细胞中瞬时表达的L1-ORF1蛋白,而且可检测出肿瘤细胞中天然表达的L1-ORF1蛋白。结论:制备的多克隆抗体具有较高的敏感性与特异性,为以后该抗体的进一步应用奠定了基础。     

Regulation of PCTAIRE1 protein stability by AKT1, LKB1 and BRCA1

PCTAIRE1, also known as CDK16, is a cyclin-dependent kinase that is regulated by cyclin Y. It is a member of the serine-threonine family of kinases and its functions have primarily been implicated in cellular processes like vesicular transport, neuronal growth and development, myogenesis, spermatogenesis and cell proliferation. However, as extensive studies on PCTAIRE1 have not yet been conducted, the signaling pathways for this kinase involved in governing many cellular processes are yet to be elucidated in detail. Here, we report the association of PCTAIRE1 with important cellular proteins involved in major cell signaling pathways, especially cell proliferation. In particular, here we show that PCTAIRE1 interacts with AKT1, a key player of the PI3K signaling pathway that is responsible for promoting cell survival and proliferation. Our studies show that PCTAIRE1 is a substrate of AKT1 that gets stabilized by it. Further, we show that PCTAIRE1 also interacts with and is degraded by LKB1, a kinase that is known to suppress cellular proliferation and also regulate cellular energy metabolism. Moreover, our results show that PCTAIRE1 is also degraded by BRCA1, a well-known tumor suppressor. Together, our studies highlight the regulation of PCTAIRE1 by key players of the major cell signaling pathways involved in regulating cell proliferation, and therefore, provide crucial links that could be explored further to elucidate the mechanistic role of PCTAIRE1 in cell proliferation and tumorigenesis.     

Antagonism between Cry1Ac1 and Cyt1A1 Toxins of Bacillus thuringiensis

Most strains of the insecticidal bacterium Bacillus thuringiensis have a combination of different protoxins in their parasporal crystals. Some of the combinations clearly interact synergistically, like the toxins present in B. thuringiensis subsp. israelensis. In this paper we describe a novel joint activity of toxins from different strains of B. thuringiensis. In vitro bioassays in which we used pure, trypsin-activated Cry1Ac1 proteins from B. thuringiensis subsp. kurstaki, Cyt1A1 from B. thuringiensis subsp. israelensis, and Trichoplusia ni BTI-Tn5B1-4 cells revealed contrasting susceptibility characteristics. The 50% lethal concentrations (LC₅₀s) were estimated to be 4,967 of Cry1Ac1 per ml of medium and 11.69 ng of Cyt1A1 per ml of medium. When mixtures of these toxins in different proportions were assayed, eight different LC₅₀s were obtained. All of these LC₅₀s were significantly higher than the expected LC₅₀s of the mixtures. In addition, a series of bioassays were performed with late first-instar larvae of the cabbage looper and pure Cry1Ac1 and Cyt1A1 crystals, as well as two different combinations of the two toxins. The estimated mean LC₅₀ of Cry1Ac1 was 2.46 ng/cm² of diet, while Cyt1A1 crystals exhibited no toxicity, even at very high concentrations. The estimated mean LC₅₀s of Cry1Ac1 crystals were 15.69 and 19.05 ng per cm² of diet when these crystals were mixed with 100 and 1,000 ng of Cyt1A1 crystals per cm² of diet, respectively. These results indicate that there is clear antagonism between the two toxins both in vitro and in vivo. Other joint-action analyses corroborated these results. Although this is the second report of antagonism between B. thuringiensis toxins, our evidence is the first evidence of antagonism between toxins from different subspecies of B. thuringiensis (B. thuringiensis subsp. kurstaki and B. thuringiensis subsp. israelensis) detected both in vivo and in vitro. Some possible explanations for this relationship are discussed.     

Role of the ASK1-SEK1-JNK1-HIPK1 signal in Daxx trafficking and ASK1 oligomerization

Overexpression of JNK binding domain inhibited glucose deprivation-induced JNK1 activation, relocalization of Daxx from the nucleus to the cytoplasm, and apoptosis signal-regulating kinase 1 (ASK1) oligomerization in human prostate adenocarcinoma DU-145 cells. However, SB203580, a p38 inhibitor, did not prevent relocalization of Daxx and oligomerization of ASK1 during glucose deprivation. Studies from in vivo labeling and immune complex kinase assay demonstrated that phosphorylation of Daxx occurred during glucose deprivation, and its phosphorylation was mediated through the ASK1-SEK1-JNK1-HIPK1 signal transduction pathway. Data from immunofluorescence staining and protein interaction assay suggest that phosphorylated Daxx may be translocated to the cytoplasm, bind to ASK1, and subsequently lead to ASK1 oligomerization. Mutation of Daxx Ser667 to Ala results in suppression of Daxx relocalization during glucose deprivation, suggesting that Ser667 residue plays an important role in the relocalization of Daxx. Unlike wild-type Daxx, a Daxx deletion mutant (amino acids 501-625) mainly localized to the cytoplasm, where it associated with ASK1, activated JNK1, and induced ASK1 oligomerization without glucose deprivation. Taken together, these results show that glucose deprivation activates the ASK1-SEK1-JNK1-HIPK1 pathway, and the activated HIPK1 is probably involved in the relocalization of Daxx from the nucleus to the cytoplasm. The relocalized Daxx may play an important role in glucose deprivation-induced ASK1 oligomerization.     

Antagonism between Cry1Ac1 and Cyt1A1 toxins of bacillus thuringiensis

Most strains of the insecticidal bacterium Bacillus thuringiensis have a combination of different protoxins in their parasporal crystals. Some of the combinations clearly interact synergistically, like the toxins present in B. thuringiensis subsp. israelensis. In this paper we describe a novel joint activity of toxins from different strains of B. thuringiensis. In vitro bioassays in which we used pure, trypsin-activated Cry1Ac1 proteins from B. thuringiensis subsp. kurstaki, Cyt1A1 from B. thuringiensis subsp. israelensis, and Trichoplusia ni BTI-Tn5B1-4 cells revealed contrasting susceptibility characteristics. The 50% lethal concentrations (LC50s) were estimated to be 4,967 of Cry1Ac1 per ml of medium and 11.69 ng of Cyt1A1 per ml of medium. When mixtures of these toxins in different proportions were assayed, eight different LC50s were obtained. All of these LC50s were significantly higher than the expected LC50s of the mixtures. In addition, a series of bioassays were performed with late first-instar larvae of the cabbage looper and pure Cry1Ac1 and Cyt1A1 crystals, as well as two different combinations of the two toxins. The estimated mean LC50 of Cry1Ac1 was 2.46 ng/cm2 of diet, while Cyt1A1 crystals exhibited no toxicity, even at very high concentrations. The estimated mean LC50s of Cry1Ac1 crystals were 15.69 and 19.05 ng per cm2 of diet when these crystals were mixed with 100 and 1,000 ng of Cyt1A1 crystals per cm2 of diet, respectively. These results indicate that there is clear antagonism between the two toxins both in vitro and in vivo. Other joint-action analyses corroborated these results. Although this is the second report of antagonism between B. thuringiensis toxins, our evidence is the first evidence of antagonism between toxins from different subspecies of B. thuringiensis (B. thuringiensis subsp. kurstaki and B. thuringiensis subsp. israelensis) detected both in vivo and in vitro. Some possible explanations for this relationship are discussed.     

Characterization of Chrysanthemum ClSOC1-1 and ClSOC1-2, homologous genes of SOC1

The MADS-box gene SOC1/TM3 (SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1/ Tomato MADS-box gene 3) is a main integrator in the Arabidopsis flowering pathway; its structure and function are highly conserved in many plant species. SOC1-like genes have been isolated in chrysanthemum, one of the most well-known ornamental plants, but it has not been well characterized thus far. We isolated and characterized ClSOC1-1 and ClSOC1-2, two putative orthologs of Arabidopsis SOC1, from the wild diploid chrysanthemum, Chrysanthemum lavandulifolium, to investigate the regulatory mechanisms of flowering time control in chrysanthemum. Expression analysis indicated that ClSOC1-1 and ClSOC1-2 were expressed in all examined organs/tissues (leaves, shoot apices, petioles, stems and roots) with different expression levels, and with high expression in the shoot apices and leaves during the early stage of floral transition. The expression levels of ClSOC1-1 and ClSOC1-2 in the shoot apices increased at different developmental stages with the highest expression levels after 7 days of short-day treatment. Overexpression of ClSOC1-1 and ClSOC1-2 in wild-type Arabidopsis resulted in early flowering, which was coupled with the upregulation of one of the flowering promoter genes LEAFY. Our results suggested that the ClSOC1-1 and ClSOC1-2 genes play an evolutionarily conserved role in promoting flowering in Chrysanthemum lavandulifolium and could serve as a vital target for the genetic manipulation of flowering time in the chrysanthemum.