航天搭载对武夷名丛相关生理及生长特性的影响

以神舟八号飞船搭载的6种武夷名丛种子SP₁代株系为材料, 探讨航天搭载对武夷名丛SP₁代株系叶片形态、光合色素含量、叶绿素荧光参数、可溶性糖和蛋白质含量以及茶叶品质成分含量的影响, 分析航天搭载后武夷名丛生长和生理特性的变化, 从中筛选优良突变株。结果表明, 航天搭载后6个武夷名丛SP₁代植株的叶长、叶宽、节间长度和叶面积均发生变化, 其中, 雀舌、肉桂和奇丹的叶面积显著增加; 航天搭载显著提高雀舌、奇丹、肉桂和金毛猴的叶绿素及类胡萝卜素含量, 瞬时叶绿素荧光(F_t)和光量子效率(Qy)也有所增加, 这有利于提高光合效率; 武夷名丛航天搭载后表现出可溶性糖含量增加而蛋白质含量减少, 氨基酸和茶多酚含量下降, 儿茶素和咖啡碱含量上升。综合各项指标, 航天搭载后6个武夷名丛中雀舌可以作为有益变异株系加以选育。     

寒地不同熟性品种水稻产量对CO2浓度和温度升高响应的模拟

选择黑龙江省作为研究区域,根据主栽水稻生育期内所需积温选取3个代表性品种,重点分析增温和大气CO₂肥效作用对不同熟性品种水稻产量的影响.采用2013年的逐日气象资料及开顶式气室(OTC)(3个CO₂浓度:390、450和550 μmol·mol^-1)试验资料对品种的遗传参数进行调试;然后采用经验证的CERES-Rice作物模型分别模拟了3个CO₂浓度水平下,伴随温度升高1、2、3和4 ℃时早、中、晚熟品种水稻产量.结果表明: 随CO₂浓度升高,不同品种水稻产量均上升;随温度升高,早熟品种产量持续下降,中、晚熟品种产量先上升再下降.若不考虑CO₂肥效作用,除了中熟和晚熟品种在增温1 ℃时会有3.1%和0.27%的小幅增产外,其余均表现为减产,其中早熟品种减产幅度最大,增温4 ℃时减产高达57.7%,而中熟和晚熟品种减产10%左右.若考虑CO₂肥效作用,450 μmol·mol^-1 CO₂浓度下,中熟和晚熟品种在增温2 ℃时仍增产0.75%和3.2%;550 μmol·mol^-1 CO₂浓度下,中熟品种在增温3 ℃时仍增产4.5%,晚熟品种在增温4 ℃时仍增产0.39%.而无论是否考虑CO₂肥效作用,早熟品种在增温作用下均表现大幅度减产.与不考虑CO₂肥效相比,大气CO₂肥效作用有效提高了水稻产量,但CO₂肥效对增产的贡献率在不同品种间差异不明显,且贡献率均小于10%.     

春小麦对不同灌水处理的气孔反应及其影响因子

选用3个春小麦品种（系）,采用大田试验方法,在冬灌1800 m³·hm^-2的基础上,在生育期设3次灌水处理（T₁）、2次灌水处理（T₂）和1次灌水处理（T₃）,每次灌水1050 m³·hm^-2,研究土壤水分对春小麦生育期气孔导度的影响及气孔导度与相关环境因素的关系.结果表明：灌水处理对春小麦生育期气孔导度的影响较大,气孔导度随着灌溉次数的减少逐渐降低,同时不同基因型间存在差异.从拔节期到开花期,不同处理春小麦气孔导度变化一致,都呈先升高后降低趋势, 在抽穗期达到峰值;开花期之后各处理出现差异,T₁各品种气孔导度先下降后上升,T₂品种间表现不同,T₃一直呈下降趋势.各环境因子中,大气相对湿度对春小麦气孔导度的影响最大,两者的相关系数在T₂和T₃中分别达显著(0.82^*)和极显著水平(0.92^**).春小麦适应水分亏缺的气孔调节机理为反馈式调节.     

施氮量对不同藜麦品种幼苗生长的影响

通过盆栽试验,研究5个水平的施氮量(N₀,0 g·kg^-1;N₁,0.05 g·kg^-1;N₂,0.1 g·kg^-1;N₃,0.15 g·kg^-1;N₄,0.2 g·kg^-1)对8个不同藜麦品种幼苗生长的影响。结果表明: 1)不同施氮量处理下,藜麦品种GB22和OY的生物量最大,而品种B2的生物量最小。品种B2的花质量比最大,品种GB22的茎质量比最大,品种R1的根质量比最大,品种W23的叶质量比最大。2)施氮显著影响藜麦幼苗的生长。在较低施氮量(N₁、N₂)下,叶片最大净光合速率、植株生物量积累都比对照(N₀)明显增加;在较高施氮量(N₃、N₄)下,藜麦叶片光合速率出现降低趋势,生物量积累减少。品种和施氮量对植株生物量有显著的交互作用,表明不同藜麦品种对施氮量的响应不同。品种R1、MY11、GB22、OY的最佳施氮量为0.05 g·kg^-1,品种GB11、DB、B2的最佳施氮量为0.1 g·kg^-1,品种W23的最佳施氮量小于0.05 g·kg^-1。3)品种和施氮量之间的交互作用显著影响藜麦幼苗的生物量分配。在达到0.2 g·kg^-1施氮量前,随着施氮量增加,藜麦将更多的生物量分配到花和叶。4)不同品种和施氮量下,幼苗生物量与最大净光合速率、苗高、地径、比叶面积呈显著正相关。本研究可为不同藜麦品种的养分管理提供参考。     

水稻两性生殖细胞的N-甲基-N-亚硝基脲诱变方法

N-甲基-N-亚硝基脲(MNU)被用于水稻(Oryza sativa)受精卵的诱变。通过水稻辽盐6号成熟生殖器官的MNU体内同步处理及后代群体筛查, 确立了水稻两性生殖细胞的MNU诱变方法。与辽盐6号受精卵的MNU处理相比, 各组条件下两性生殖细胞的MNU处理明显使M₁群体生长发育的指标降低及M₁-M₂群体中突变性状的发生率升高。两性生殖细胞在含有1.5 mmol?L ^-1 MNU和10 mmol?L ^-1 PO₄ ^3-的缓冲液(pH4.8)中处理60分钟, 突变性状发生率是基于受精卵MNU处理的3倍。进一步筛查M₃群体, 获得了包含新型植株和籽粒突变体的纯合突变体系列。研究结果表明, 水稻两性生殖细胞的MNU诱变可显著提高广谱诱变效率。该技术的应用可为水稻的未知功能基因鉴定和育种所需的各种突变体规模化开发提供高效的技术支撑。     

水稻两性生殖细胞的N-甲基-N-亚硝基脲诱变方法

N-甲基-N-亚硝基脲(MNU)被用于水稻(Oryza sativa)受精卵的诱变。通过水稻辽盐6号成熟生殖器官的MNU体内同步处理及后代群体筛查, 确立了水稻两性生殖细胞的MNU诱变方法。与辽盐6号受精卵的MNU处理相比, 各组条件下两性生殖细胞的MNU处理明显使M₁群体生长发育的指标降低及M₁-M₂群体中突变性状的发生率升高。两性生殖细胞在含有1.5 mmol∙L ^-1 MNU和10 mmol∙L ^-1 PO₄ ^3-的缓冲液(pH4.8)中处理60分钟, 突变性状发生率是基于受精卵MNU处理的3倍。进一步筛查M₃群体, 获得了包含新型植株和籽粒突变体的纯合突变体系列。研究结果表明, 水稻两性生殖细胞的MNU诱变可显著提高广谱诱变效率。该技术的应用可为水稻的未知功能基因鉴定和育种所需的各种突变体规模化开发提供高效的技术支撑。     

红掌组织培养与快速繁殖

红掌叶片在新代培养基上的分化能力与品种和叶片部位有关。组织培养试验表明,最佳诱导培养基为改良Nitsch (NH₄NO₃ 200mg/L)+6-BA 1.0mg/L+2,4-D 0.1mg/L;芽增殖培养基Nitsch (NH₄NO₃720mg/L)+6-BA 0.5mg/L;生根培养基为Nitsch (NH₄NO₃720mg/L)。     

冬小麦幼苗生长和化感物质对CO2和O3浓度升高的响应

利用开顶式气室(OTC), 采用盆栽试验研究了CO₂浓度为550 μL·L^-1、O₃浓度为60 μL·L^-1及CO₂浓度为550 μL·L^-1+O₃浓度为60 μL·L^-1对7个冬小麦品种幼苗生物量和化感物质丁布(DIMBOA)的影响.结果表明：在高CO₂浓度下,冬小麦幼苗地上生物量与丁布含量在品种间存在显著差异,品种碧蚂1号幼苗和根干质量比对照（CO₂浓度为370 μL·L^-1,O₃浓度为40 μL·L^-1）增加了36.8%和24.7%;丁布含量增幅为5.7%~184.6%.除碧蚂1号和陕139外,高浓度O₃导致冬小麦生物量降低,但使所有品种丁布含量显著增加,变幅为0.5~3倍.交互作用下所有品种根干质量降低,长武134地上部质量、根质量和丁布含量降幅最大,分别为82%、27.9%和35.5%;与长武134、远丰175和兰考217丁布含量降低相反,陕139丁布含量增加84.6%.聚类分析显示,不同处理和不同品种均显著影响丁布含量,陕139、兰考217和长武134在高CO₂和O₃浓度处理下聚为一类,而陕139在所有处理中丁布含量均表现为增加.表明化感物质丁布可以作为气候变化条件下,尤其是CO₂和O₃变化下抗性育种的特定指标.     

转基因抗虫棉对不同生态环境的适应性研究

选用7个转基因抗虫棉品种WH₁、WH₂ 、WH₃ 、WH₄ 、WH₅、WH₆、BG₂ 和一个常规种泗棉 3号 (CK),在10个生态环境不同的试验点,对它们的抗虫特性和产量性状的适应性进行了研究.结果表明,转基因抗虫棉对棉铃虫 (Helicoverpa armigera)、棉红铃虫 (Pectinophora gossypiella)抗性很强,并且不受生态环境差异的影响,稳定程度较高.但其产量性状受环境影响较大,品种和试验点的互作效应显著.与对照相比,WH₆和BG₂ 的抗虫性和丰产性较好,可以在生产上应用.     

冬小麦幼苗生长和化感物质对CO2和O3浓度升高的响应

利用开顶式气室(OTC), 采用盆栽试验研究了CO₂浓度为550 μL·L^-1、O₃浓度为60 μL·L^-1及CO₂浓度为550 μL·L^-1+O₃浓度为60 μL·L^-1对7个冬小麦品种幼苗生物量和化感物质丁布(DIMBOA)的影响.结果表明：在高CO₂浓度下,冬小麦幼苗地上生物量与丁布含量在品种间存在显著差异,品种碧蚂1号幼苗和根干质量比对照（CO₂浓度为370 μL·L^-1,O₃浓度为40 μL·L^-1）增加了36.8%和24.7%;丁布含量增幅为5.7%~184.6%.除碧蚂1号和陕139外,高浓度O₃导致冬小麦生物量降低,但使所有品种丁布含量显著增加,变幅为0.5~3倍.交互作用下所有品种根干质量降低,长武134地上部质量、根质量和丁布含量降幅最大,分别为82%、27.9%和35.5%;与长武134、远丰175和兰考217丁布含量降低相反,陕139丁布含量增加84.6%.聚类分析显示,不同处理和不同品种均显著影响丁布含量,陕139、兰考217和长武134在高CO₂和O₃浓度处理下聚为一类,而陕139在所有处理中丁布含量均表现为增加.表明化感物质丁布可以作为气候变化条件下,尤其是CO₂和O₃变化下抗性育种的特定指标.     

空间诱变条件下蜜蜂后代的波动性不对称

利用航天搭载的雄蜂精液对处女王进行人工授精,产卵后大量培育后代蜂王;以SP1、SP2及SP3代蜂王后代工蜂为研究对象,考查波动性不对称(fluctuating asymmetry,FA)在不同代次种群中各对称性状间的表现情况。结果表明:SP1、SP2和SP3代工蜂的前翅长及肘脉a均表现出FA,SP1、SP2代的对照组中均未出现,而SP3代的对照组蜂群则全部表现出FA;与对照蜂群相比,空间诱变后代的前翅长及翅脉a的FA值均较高。此外,讨论FA在蜜蜂种群对生态环境适应性上应用以及利用蜜蜂的FA来监测环境污染的可能性及发展前景。     

Glucose metabolic adaptations in the intrauterine growth-restricted adult female rat offspring

We studied glucose metabolic adaptations in the intrauterine growth-restricted (IUGR) rat offspring to decipher glucose homeostasis in metabolic programming. Glucose futile cycling (GFC), which is altered when there is imbalance between glucose production and utilization, was studied during a glucose tolerance test (GTT) in 2-day-old (n = 8), 2-mo-old (n = 22), and 15-mo-old (n = 22) female rat offspring. The IUGR rats exposed to either prenatal (CM/SP, n = 5 per age), postnatal (SM/CP, n = 6), or pre- and postnatal (SM/SP, n = 6) nutrient restriction were compared with age-matched controls (CM/CP, n = 5). At 2 days, IUGR pups (SP) were smaller and glucose intolerant and had increased hepatic glucose production and increased glucose disposal (P < 0.01) compared with controls (CP). At 2 mo, the GTT, glucose clearance, and GFC did not change. However, a decline in hepatic glucose-6-phosphatase (P < 0.05) and fructose-1,6-biphosphatase (P < 0.05) enzyme activities in the IUGR offspring was detected. At 15 mo, prenatal nutrient restriction (CM/SP) resulted in greater weight gain (P < 0.01) and hyperinsulinemia (P < 0.001) compared with postnatal nutrient restriction (SM/CP). A decline in GFC in the face of a normal GTT occurred in both the prenatal (CM/SP, P < 0.01) and postnatal calorie (SM/CP, P < 0.03) and growth-restricted offspring. The IUGR offspring with pre- and postnatal nutrient restriction (SM/SP) were smaller, hypoinsulinemic (P < 0.03), and hypoleptinemic (P < 0.03), with no change in GTT, hepatic glucose production, GFC, or glucose clearance. We conclude that there is pre- and postnatal programming that affects the postnatal compensatory adaptation of GFC and disposal initiated by changes in circulating insulin concentrations, thereby determining hepatic insulin sensitivity in a phenotype-specific manner.     

Fetal exposure to cocaine causes programming of Prkce gene repression in the left ventricle of adult rat offspring

Previous studies demonstrated that maternal cocaine administration caused a significant decrease in protein kinase C epsilon (PRKCE) abundance in the left ventricle and an increase in susceptibility of the heart to ischemic injury in adult male offspring. The present study tested the hypothesis that epigenetic modification has a key role in cocaine-mediated programming of cardiac Prkce gene repression. Pregnant Sprague-Dawley rats were administered saline or cocaine (30 mg/kg/day i.p.) from Days 15 to 21 of gestational age, and hearts of 3-mo-old adult offspring were studied. Cocaine exposure significantly decreased Prkce mRNA levels in the left ventricle of male but not female offspring. CpG dinucleotides identified in Bhlhb2, Pparg, E2f, and Egr1 binding sites at the Prkce gene promoter were densely methylated in males and females and were unaffected by cocaine exposure. In contrast, methylation of CpGs in the two Sp1 binding sites (-346 and -268) was low and was significantly increased by cocaine exposure in male offspring. In females, methylation of the Sp1 binding site at -268 but not -346 was increased. Reporter gene assays showed that both Sp1 binding sites had a strong stimulatory role in Prkce gene activity. Methylation of the Sp1 binding sites significantly decreased SP1 binding to the Prkce promoter. Cocaine exposure did not affect nuclear SP1 protein levels but decreased the SP1 binding affinity to its binding site at -268. The results demonstrate an epigenetic mechanism of DNA methylation in programming of cardiac Prkce gene repression, linking fetal cocaine exposure and pathophysiological consequences in the heart of adult male offspring in a gender-dependent manner.     

Perturbed skeletal muscle insulin signaling in the adult female intrauterine growth-restricted rat

To determine the molecular mechanism(s) linking fetal adaptations in intrauterine growth restriction (IUGR) to adult maladaptations of type 2 diabetes mellitus, we investigated the effect of prenatal seminutrient restriction, modified by early postnatal ad libitum access to nutrients (CM/SP) or seminutrient restriction (SM/SP), vs. early postnatal seminutrient restriction alone (SM/CP) or control nutrition (CM/CP) on the skeletal muscle postreceptor insulin-signaling pathway in the adult offspring. The altered in utero hormonal/metabolic milieu was associated with no change in basal total IRS-1, p85, and p110beta subunits of PI 3-kinase, PKCtheta, and PKCzeta concentrations but an increase in basal IRS-2 (P < 0.05) only in the CM/SP group and an increase in basal phospho (p)-PDK-1 (P < 0.05), p-Akt (P < 0.05), and p-PKCzeta (P < 0.05) concentrations in the CM/SP and SM/SP groups. Insulin-stimulated increases in p-PDK-1 (P < 0.05) and p-Akt (P < 0.0007), with no increase in p-PKCzeta, were seen in both CM/SP and SM/SP groups. SHP2 (P < 0.03) and PTP1B (P < 0.03) increased only in SM/SP with no change in PTEN in CM/SP and SM/SP groups. Aberrations in kinase and phosphatase moieties in the adult IUGR offspring were initiated in utero but further sculpted by the early postnatal nutritional state. Although the CM/SP group demonstrated enhanced kinase activation, the SM/SP group revealed an added increase in phosphatase concentrations with the net result of heightened basal insulin sensitivity in both groups. The inability to further respond to exogenous insulin was due to the key molecular distal roadblock consisting of resistance to phosphorylate and activate PKCzeta necessary for GLUT4 translocation. This protective adaptation may become maladaptive and serve as a forerunner for gestational and type 2 diabetes mellitus.     

高表达人源SP15对小鼠生长和生殖的影响

目的:探究高表达人源SP15对小鼠生长和生殖的影响,为研究NYD-SP15在生物体中的功能提供动物模型。方法:将人源NYD-SP15 cDNA以及Cre序列插入PCAG启动子下游,构建NYD-SP15转基因表达载体,并通过原核注射,构建全身性表达NYD-SP15的转基因小鼠;将获得的NYD-SP15转基因小鼠与C57/BL6小鼠交配,PCR鉴定转基因小鼠是否有Cre插入,筛选出人源NYD-SP15表达的小鼠,统计转基因小鼠体重变化和后代阳性情况。结果:通过PCR鉴定及公司测序验证,我们成功构建了NYD-SP15转基因过表达载体。并通过PCR鉴定小鼠基因型,筛选出可以表达人NYD-SP15的转基因小鼠。比较转基因小鼠与同窝野生型小鼠体重,发现转基因小鼠体重与同窝野生型小鼠相比无明显区别,说明在体内过表达NYD-SP15对小鼠体重无明显影响。通过对后代阳性小鼠出生情况统计发现F2代阳性小鼠出生率较F1代明显降低。结论:人源NYD-SP15在小鼠体内能正常表达,对其生长无明显影响,但其后代阳性出生率呈逐代下降趋势,推测该原因可能与NYD-SP15在睾丸中表达有关。     

Pro-inflammatory effects of hydrogen sulphide on substance P in caerulein-induced acute pancreatitis

Hydrogen sulphide (H(2)S), a novel gasotransmitter, has been recognized to play an important role in inflammation. Cystathionine-gamma-lyase (CSE) is a major H(2)S synthesizing enzyme in the cardiovascular system and DL-propargylglycine (PAG) is an irreversible inhibitor of CSE. Substance P (SP), a product of preprotachykinin-A (PPT-A) gene, is a well-known pro-inflammatory mediator which acts principally through the neurokinin-1 receptor (NK-1R). We have shown an association between H(2)S and SP in pulmonary inflammation as well as a pro-inflammatory role of H(2)S and SP in acute pancreatitis. The present study was aimed to investigate the interplay between pro-inflammatory effects of H(2)S and SP in a murine model of caerulein-induced acute pancreatitis. Acute pancreatitis was induced in mice by 10 hourly intraperitoneal injections of caerulein (50 (g/kg). PAG (100 mg/kg, i.p.) was administered either 1 hr before (prophylactic) or 1 hr after (therapeutic) the first caerulein injection. PAG, given prophylactically as well as therapeutically, significantly reduced plasma H(2)S levels and pancreatic H(2)S synthesizing activities as well as SP concentrations in plasma, pancreas and lung compared with caerulein-induced acute pancreatitis. Furthermore, prophylactic as well as therapeutic administration of PAG significantly reduced PPT-A mRNA expression and NK-1R mRNA expression in both pancreas and lung when compared with caerulein-induced acute pancreatitis. These results suggest that the pro-inflammatory effects of H(2)S may be mediated by SP-NK-1R pathway in acute pancreatitis.     

The secretion of parathormone and glycosylated proteins by parathyroid cells in culture

The secretion of radioactive peptides by dispersed porcine parathyroid cells incubated with [³H]- or [¹⁴C]amino acids, [³H]glucosamine and [³H]mannose was analyzed. After incubation, the culture medium contained radioactive parathormone, as expected, and two radioactive glycopeptides: SP I and SP II. SP I appears to be identical with $\text{parathyroid}\text{secretory}\text{protein}$, heretofore not recognized as a glycoprotein. SP II has not been previously identified. SP I, but not SP II or parathormone, was adsorbed by Concanavalin A possibly reflecting a high mannose content of this molecule. Raising the concentration of calcium in the medium suppressed the secretion of radioactive parathormone and SP I in a similar fashion but did not affect the secretion of SP II. Our results suggest that SP I may play a fundamental role in parathyroid synthetic or secretory processes.     

Maternal betaine supplementation attenuates glucocorticoid-induced hepatic lipid accumulation through epigenetic modification in adult offspring rats

There are lots of reports about alleviation of NAFLD by dietary supplements of betaine. However, it remains unclear whether maternal betaine supplementation can also ameliorate NAFLD in offspring. Hence, twenty pregnant rats were fed with a basal diet with or without betaine (1%), and then the female offspring rats were raised at 3 months of age followed by 3 weeks of physiological saline or dexamethasone in a dose of 0.1 mg/kg body mass every day via intraperitoneal injection. In this study, maternal betaine supplementation significantly (P<.05) reduced the increase of hepatic triglycerides concentration in dexamethasone-induced rats, which is associated with the expression of hepatic lipogenic genes (ACC1, FASN and SCD1). Moreover, the hypomethylation of lipogenic genes in dexamethasone-induced rats were reserved by prenatal betaine exposure. Furthermore, the increase of hepatic GR or SP1 content in dexamethasone-injected rats were significantly decreased (P<.05), which were in line with the binding of GR or SP1 to lipogenic genes, in betaine -exposed rats. Together, these results suggest that maternal betaine supplementation attenuates dexamethason-induced fatty liver in the female adult offspring rats, which may be attributed to DNA methylation and GR or SP1-mediated the regulation of lipogenic genes.