农垦58s光敏不育基因在水稻第5染色体上位置的确定

利用３个带有第５染色体上标记基因的标记基因系，采用ＢＣ１Ｆ２株系分析，对农垦５８ｓ的１对光敏感雄性不育基因在第５染色体上的位置进行了定位。结果表明，农垦５８ｓ的１对光敏感雄性不育基因与第５染色体上的ｇｈ－１基因以２０．３ｃＭ的遗传图距连锁遗传，与ｎｌ－１，ｖ－１０基因的遗传图距较远，在分离群体中不能发现其连锁遗传关系。将农垦５８ｓ的１对光敏感雄性不育基因定位于水稻第５染色体上端。     

吉密豆1号矮秆性状遗传规律分析

[目的]探明吉密豆1号矮秆性状的遗传规律。[方法]以吉密豆1号（矮秆,母本）、吉育47（株高正常,父本）、辽豆14（株高较高,父本）及其杂交F1、F2代和回交BC1、BC2代为材料,研究吉密豆1号矮秆基因的遗传规律。[结果]F1代平均株高均高于中亲值,矮秆性状表现为隐性;杂交组合（吉密豆1号×吉育47、吉密豆1号×辽豆14）与双亲回交世代株高的分离比例符合1对基因控制性状的分离比例;2个组合R代株高的分离比例为3：1。[结论]吉密豆1号的矮秆性状受1对隐性基因控制。     

Prevention of type I diabetes in nonobese diabetic mice by virus infection

The nonobese diabetic (NOD) mouse is an animal model of type I diabetes and develops a characteristic autoimmune lesion in the islets of Langerhans with lymphocytic infiltration and destruction of pancreatic beta cells. The result is hypoinsulinemia, hyperglycemia, ketoacidosis, and death. Diabetes usually begins by the sixth month of age but can occur earlier when young NOD mice are infused with lymphocytes from older NOD donors. When newborn or adult NOD mice were infected with a lymphotropic virus they did not become diabetic. The interaction between viruses and lymphocytes is pivotal in aborting diabetes, as established by experiments in which lymphocytes from virus-infected donors failed to transfer diabetes. In contrast, lymphocytes from age- and sex-matched uninfected donors caused disease. Therefore, viruses and, presumably, their products can be developed to be beneficial and may have potential as a component for treatment of human diseases. Further, these results point to the utility of viruses as probes for dissecting the pathogenesis of a nonviral disease.     

甘蔗与斑茅割手密复合体的回交后代真实性鉴定及染色体遗传分析

【目的】掌握斑茅割手密复合体(简称斑割复合体)在杂交利用过程中的染色体遗传规律,为斑割复合体适宜回交利用代数提供参考依据。【方法】选用4对引物对甘蔗与斑茅割手密复合体的回交后代进行SSR标记鉴定,并利用甘蔗根尖细胞酶解去壁低渗法对真实杂种进行染色体数目观察。【结果】供试的28个杂交后代材料(15个GT05-164与GXASF108-2-28杂交BC1代,13个GT42与GXASBC112-A6-25杂交BC2代)均为真实杂种。选择在2对SSR引物中均扩增出父本特征带的后代(5个BC1代和7个BC2代)进行染色体观察,结果发现,5个BC1代的染色体数目介于95~98条,其染色体按“n+n”方式传递;7个BC2代的染色体数目介于94~101条,其染色体也按“n+n”方式传递。【结论】甘蔗与斑割复合体杂交BC1和BC2代中染色体传递方式均为“n+n”,母本甘蔗的染色体未加倍,高贵化育种进程减慢,可能需要更高的杂交代数才能获得聚集斑茅和割手密血缘的优良品种(系)。     

The NOD mouse: recessive diabetogenic gene in the major histocompatibility complex

Examination of the histocompatibility region of the nonobese diabetic (NOD) mouse with antibodies against class II glycoproteins (products of immune response genes of the major histocompatibility complex I-A and I-E), hybrid T-cell clones, and mixed-lymphocyte cultures and analysis of restriction fragment length polymorphisms indicate that the NOD mouse has a unique class II major histocompatibility complex with no expression of surface I-E, no messenger RNA for I-E alpha, and an I-A not recognized by any monoclonal antibodies or hybrid T-cell clones studied. In crosses of NOD mice with control C3H mice, the development of diabetes was dependent on homozygosity for the NOD mouse's unique major histocompatibility region.     

MHC-linked protection from diabetes dissociated from clonal deletion of T cells

The I-E molecule of the major histocompatibility complex (MHC) can prevent the spontaneous development of diabetes in nonobese diabetic (NOD) mice. The mechanism of this protection has been investigated by breeding wild-type and promoter-mutated E kappa alpha transgenes onto the NOD genetic background. Animals carrying the various mutated transgenes expressed I-E on different subsets of immunocompetent cells, and thus cells important for the I-E protective effect could be identified. Although the wild-type transgene prevented the infiltration of lymphocytes into pancreatic islets, none of the mutants did. However, all of the transgenes could mediate the intrathymic elimination of T cells bearing antigen receptors with variable regions that recognize I-E. Thus, the I-E molecule does not protect NOD mice from diabetes simply by inducing the deletion of self-reactive T cells.     

Nod2 mutation in Crohn's disease potentiates NF-kappaB activity and IL-1beta processing

Variants of NOD2, an intracellular sensor of bacteria-derived muramyl dipeptide (MDP), increase susceptibility to Crohn's disease (CD). These variants are thought to be defective in activation of nuclear factor kappaB (NF-kappaB) and antibacterial defenses, but CD clinical specimens display elevated NF-kappaB activity. To illuminate the pathophysiological function of NOD2, we introduced such a variant to the mouse Nod2 locus. Mutant mice exhibited elevated NF-kappaB activation in response to MDP and more efficient processing and secretion of the cytokine interleukin-1beta (IL-1beta). These effects are linked to increased susceptibility to bacterial-induced intestinal inflammation and identify NOD2 as a positive regulator of NF-kappaB activation and IL-1beta secretion.     

水稻抗白叶枯病近等基因系CBB30的培育及Xa30(t)的初步定位

 【目的】将普通野生稻资源Y238所携有的抗白叶枯病新基因Xa30(t)导入栽培稻JG30，培育近等基因系，进行分子标记定位，以便应用于育种实践。【方法】以感病籼稻品种JG30为轮回亲本，Y238为供体进行杂交、回交、自交培育近等基因系；以JG30/Y238的一个BC6F2代群体为定位群体，利用分离集团分析法（BSA），借助SSR、EST、STS等分子标记对Xa30(t)进行分子标记定位。【结果】成功培育了携有Xa30(t)基因的水稻抗白叶枯病近等基因系CBB30。从343个分子标记中筛选出4个能揭示抗感多态性的标记RM1341、V88、C189及03STS，用该4个标记对BC6F2代群体303个单株进行分子检测和连锁分析，结果表明上述4个标记均位于水稻第11染色体长臂，与Xa30(t)的遗传距离分别为11.4 cM、11.4 cM、4.4 cM及2.0 cM，且它们位于Xa30(t)基因的同一侧。【结论】通过构建近等基因系及分子标记检测找到4个与Xa30(t)基因连锁的标记RM1341、V88、C189及03STS，将Xa30(t)基因定位于水稻第11染色体长臂上。     

籼型红米具有的恢复性及其基因定位

经四川农业大学水稻研究所良繁研究室发现,（G46A、D702A、珍汕97A）D 62A／红宝石的F1代,植株基本全不育,但在回交过程中育性发生分离,可育株数明显增多,猜想红宝石具有对G46A、D702A、珍汕97A和D62A育性恢复的特性。为了验证该猜想,笔者构建遗传群体对其恢复性进行分析,并用SSLP对红宝石的恢复基因加以定位。     

Ogura雄性不育甘蓝型油菜×白菜、芜菁杂种F1及其回交后代染色体减数分裂行为分析

 以甘蓝型油菜（Brassica napus L.，AACC，2n＝38）Ogura CMS材料与白菜 （B. campestris ssp. chinensis Makino, AA，2n＝20） 品种新选1号、矮脚黄和芜菁 （B. campestris ssp. rapifera Sinsk , AA，2n＝20）品种耐病98-1进行杂交、回交。F1花粉母细胞减数分裂染色体构型为10Ⅱ+9Ⅰ。BC1生长势强的群体中，新选1号和耐病98-1染色体构型多为10Ⅱ+9Ⅰ，矮脚黄的染色体构型以10Ⅱ和10Ⅱ+7Ⅰ占优势；BC1生长势弱的群体中，新选1号和耐病98-1染色体构型多为10Ⅱ+7Ⅰ，矮脚黄的染色体构型多为10Ⅱ+1Ⅰ。BC2生长势强的群体中，新选1号的染色体构型多为10Ⅱ+1Ⅰ，矮脚黄多为10Ⅱ；BC2生长势弱的群体中，新选1号和矮脚黄多为10Ⅱ，耐病98-1多为10Ⅱ+6Ⅰ、10Ⅱ+5Ⅰ。BC3根尖染色体观察新选1号、矮脚黄染色体数达到100%，耐病98-1中染色体数为20的细胞达到78.12%。同时对BC1代不同染色体数在减数分裂Ⅰ的分离规律进行了研究。结果表明，AACC染色体组物种与AA染色体组物种杂交经少数几代回交即可获得后代性状相对稳定的不育系。     

烟草品种Coker176和Ti245抗TMV的遗传分析*

 以2个抗烟草花叶病毒（TMV）的烟草品种Coker176和Ti245及感TMV烟草品种K326为材料,经杂交、自交、回交建立F1,F2,BC1等世代群体。采用人工接种TMV的方法对各群体进行抗性鉴定,统计各世代抗感植株数;利用卡方测验对分离世代群体进行抗感分离比检测。结果表明,Coker176的TMV抗性由一对显性基因所控制,Ti245的TMV抗性由两对隐性基因所控制。最后对2个抗性亲本在抗TMV育种中的利用进行了探讨。     

不同基因型高直链淀粉玉米的遗传效应

将3个ae基因供体亲本和8个普通玉米自交系进行回交转育,测定了自交系本身及其回交转育的BC1F1和BC1F2代的千粒质量和直链淀粉含量.结果表明,BC1F2与BC1F1相比,大多数组合的直链淀粉含量有一定程度的提高,但千粒质量有降低的趋势.在回交的早代材料中,千粒质量和直链淀粉含量无明显的相关性;不同的ae基因供体亲本在遗传背景不同的轮回亲本中的表达效果有很大的差别.     

水稻4个异交相关性状的QTL定位研究

利用由98个家系组成的Nipponbare/Kasalath//Nipponbare回交重组自交系(backcross inbred lines,BIL)作图群体(BC1F12),用复合区间作图方法(CIM),对水稻4个异交相关性状进行了QTL分析.结果表明,开颖角度检测到2个QTL,分别位于第 12 染色体的C1069-R1709和R270-G2140区间,共解释性状变异的18.51%,2个位点的增效等位基因均来自Kasalath.柱头外露率检测到1个QTL,位于第 3 染色体的C63-C563区间,解释性状变异的15.99%,增效等位基因来自Kasalath.单花开花历时检测到1个QTL,位于第9染色体的G385-R2272区间,解释性状变异的10.75%,增效等位基因来自Kasalath.包颈长检测到3个QTL,分别位于第3染色体的C136-R250、第5染色体的R521-C1230和第10染色体的R2194-R1629区间,共解释性状变异的39.40%,qPEL-5位点的增效等位基因来自Nipponbare,qPEL-3和qPEL-10位点的增效等位基因均来自Kasalath.     

Reversal of diabetes in non-obese diabetic mice without spleen cell-derived beta cell regeneration

Autoimmune destruction of beta cells is the predominant cause of type 1 diabetes mellitus (T1DM) in humans and is modeled in non-obese diabetic (NOD) mice. Many therapeutic interventions prevent the development of T1DM in NOD mice, but few can induce its reversal once established. Intervention with Freund's complete adjuvant, semi-allogeneic splenocytes, and temporary islet transplantation has been reported to cure NOD mice of established T1DM. Using the same approach, we report here that this treatment cured 32% of NOD mice of established diabetes (>340 milligrams per deciliter blood glucose), although beta cells in these mice were not derived from donor splenocytes.     

家蚕突变型灰黑蛾杂交性状调查与遗传分析

山东省蚕业研究所家蚕种质资源中保育的灰黑蛾蚕品种,其雌雄蛾体、蛾翅均为灰黑色。用灰黑蛾与白色蛾杂交,饲养F1代、F2代及BC1代,结果表明：杂交F1代全部为白色蛾;自交F2代、回交BC1代发生娥色性状分离,白蛾与灰黑蛾的分离比,F2为3：1,BC1为1：1;灰黑蛾雌雄自交,全部表现为灰黑蛾;并分析了灰黑蛾的显隐性特点及遗传规律。     

普通小麦与鹅观草杂种回交后代的赤霉病抗性及细胞遗传学研究

在普通小麦品种中国春与高抗赤霉病的亲缘物种鹅观草杂种回交后代ＢＣ２Ｆ１的基础上，对ＢＣ２Ｆ２－５，ＢＣ３Ｆ１－４等世代植株的形态，赤霉病抗性及细胞遗传学特征进行了观察及研究，结果表明：随着世代的增加，植株外部形态接近普通小麦；赤霉病抗性在高世代材料中仍得以保持；染色体数目的变异范围逐代缩小，在高世代中２ｎ＝４３，４４植株的比例增加，这展示了异附加系筛选的可喜前景     

大白菜雄性核不育基因的染色体定位及AFLP分子标记筛选

 【目的】基因定位是遗传研究的重点内容,也是育种工作的重要基础。本研究以大白菜雄性不育两用系‘大阳AB系’和大白菜系列初级三体为材料,对决定大白菜雄性不育性的核基因（ms）进行染色体定位和分子标记筛选,旨在为其分子克隆和遗传利用奠定基础。【方法】基因的染色体定位采用初级三体遗传分析和χ2测验法,分子标记采用AFLP分析方法。【结果】大白菜‘大阳AB系’的雄性不育系（msms）×大白菜系列初级三体（Tri-1、Tri-2、Tri-3、Tri-4、Tri-5、Tri-6、Tri-7、Tri-8、Tri-9）的9个杂交组合中,F1均为可育株;从F1选出三体植株进行自交和测交,其自交子代（F2）和测交子代（Tc）中可育株与不育株的分离比例,只有Tri-4表现为15.5﹕1（F2）和3.24﹕1（Tc）、不符合孟德尔的单基因遗传分离比例（3﹕1和1﹕1）,其它三体在2.60﹕1～3.76﹕1（F2）和0.81﹕1～1.48﹕1（Tc）、均符合孟德尔的单基因遗传分离比例（3﹕1和1﹕1）,这表明该雄性不育性的遗传与Tri-4的遗传表现一致,即确定该雄性不育性的基因位于大白菜4号染色体上。基于染色体和染色单体分离的三体遗传分析表明,该雄性不育基因位于4号染色体的近着丝点区域,通过对124个AFLP引物组合的筛选,初步获得了一个与雄性核不育基因位点连锁的AFLP标记E34M49(398 bp),遗传距离约为1.2 cM。【结论】利用初级三体遗传分析首次将大白菜雄性核不育基因定位在第4号染色体上。     

小菊品种‘钟山金桂’与亚菊属细裂亚菊F1 回交后代的性状遗传表现

【目的】对菊属栽培菊‘钟山金桂’与亚菊属细裂亚菊F1回交后代的性状遗传表现进行研究,获得观赏性和抗性改良的优异属间新种质。【方法】以‘钟山金桂’×细裂亚菊F1为父本,‘钟山金桂’为轮回亲本开展回交试验。对获得的回交后代进行细胞学鉴定,对BC1代的形态性状观测,对经过越冬期后田间苗脚芽萌发量进行统计分析,并对低温胁迫下植株体内生理指标进行测定。【结果】共获得17个回交后代株系。回交后代株系的形态出现分离,与亲本有显著差异,回交后代在花型上出现了托桂型、半托桂型和非托桂型的分离,大部分花型为托桂型,且部分植株花序直径大于‘钟山金桂’,回交后代所有株系的花色均为黄色。回交后代的抗寒性比‘钟山金桂’强,遗传了细裂亚菊的抗寒特性。【结论】通过回交不仅可提高远缘杂交后代的观赏品质,还从细裂亚菊获得的耐寒性也能够稳定遗传。     

小麦染色体3B和4B雌性育性遗传位点的初选

以普通小麦N8×小麦雌性不育系XND126组合衍生的F2为基本群体,从中选择100株隐性极端不育株构成极端不育群体,以2008-2010年关联分析中的38个SSR阳性关联标记为基本线索进行PCR和电泳实验。与N8带型相同的记为A;与XND126带型相同的记为B;与F1带型即杂合带型相同的记为H。以c=(N1+N2/2)/N计算c值,以c值小于0.4确定标记与位点可能的连锁关系。以初选的c值相对较小的标记为线索,在其参考连锁图上寻找并合成第二批标记引物,再次筛选,共得到3个位于3B染色体上的候选标记Xwmc687(c值为0.360),Xbarc206(c值为0.35)和Xcfb3440(c值为0.375),以及1个位于4B染色体上的候选标记Xgwm495(c值为0.295)。实验结果显示,除本实验室前期定位的小麦雌性育性2DS位点外,3B和4B上可能存在与小麦雌性育性有关的遗传位点。     

Acceleration of diabetes in young NOD mice with a CD4+ islet-specific T cell clone

Nonobese diabetic (NOD) mice develop an autoimmune form of diabetes, becoming hyperglycemic after 3 months of age. This process was accelerated by injecting young NOD mice with CD4+ islet-specific T cell clones derived from NOD mice. Overt diabetes developed in 10 of 19 experimental animals by 7 weeks of age, with the remaining mice showing marked signs of the disease in progress. Control mice did not become diabetic and had no significant pancreatic infiltration. This work demonstrates that a CD4 T cell clone is sufficient to initiate the disease process in the diabetes-prone NOD mouse.