光敏核不育水稻农垦58S与其衍生不育系的叶绿体DNA的比较

扩增了光敏核不育系农垦58S及从它衍生出来的5个两用核不育系叶绿体DNA的ORF（open reading frame）100、ORF29-TrnC^GCA、rps16（ribosomal proteins16）基因内含子和TrnT^UGU-TrnL^UAA（tRNA^Thr（UGU）-tRNA^-Leu（UAA）等4个片段,并测定了其序列。研究结果表明,粳型光敏核不系农垦58S的叶绿体为粳型。农垦58S衍生的核不育系中,粳型核不育系7001S以及3个籼型核不育系1103S、培矮64S和广占63S的叶绿体DNA为粳型,与选育者提供的细胞质系谱一致。籼型核不育系W6154S的叶绿体DNA为籼型,与选育者提供的细胞质系谱不一致,推断选育者在选育过程中更换过细胞质（曾用不育系作过父本）。5个粳型叶绿体DNA的rps16基因内含子和TrnT^UGU-TrnL^UAA间区的序列相互之间有1-2个单核苷酸的变异。     

水稻新种质明恢86及其系列组合的选育研究

通过选用籼粳交中间材料与籼型强恢材料杂交导入广亲和基因的育种方法,将粳稻基因渗入籼稻恢复系,育成的三系及二系新种质明恢86,具有广亲和性、恢复力强、恢复谱广、米质优、配合力好、抗稻瘟病、制种产量高等特点.明恢86与野败型、矮败型、K型败、印尼水田谷型、冈型败、D型败、两用不育系、新质源不育系(岳4A)等多个不育系配组,均表现出强优的杂种优势和优良的综合性状,其中汕优明86、福两优2186、Ⅱ优明86已先后通过福建省或三明市农作物品种审定委员会审定.目前,正在福建和全国南方稻区大面积推广应用.     

水稻偏粳型广谱性强恢复系种质GR38的创新和评价

用无育性恢复力的意大利粳稻巴利拉,与具有广亲和性的我国改良籼稻广中接杂交,创新出偏粳型广谱性强恢复系种质GR38。与亲本度现有4类恢复基因型仅能恢复部分不育细胞质的情况不同,GR38对几乎所有主要不育细胞质均具强恢复力。SSR标记分析发现,GR38的一个恢复基因位于第1染色体长臂中部,与已报道的恢复基因位点均有所不同,推测GR38至少携带一个新恢复基因。GR38具有很强的产量配合力,与许多不育系配制的籼粳杂交稻组合具有很强的杂种优势和产量潜力,可以直接用于生产。GR38的育成,将地理远缘的粳稻基因导入到恢复系中,创造了地理远缘粳稻／广亲和籼稻的杂交选育途径,打破了常用的籼恢／籼恢单一途径,以度恢复基因源局限于IR24度其衍生系的状况,拓宽了恢复基因源和遗传基础．有助于杂交稻育种的新突破。     

不育系培矮64S衍生的近等基因系的育性感温性及基因初定位研究

培矮64S是光敏核不育水稻农垦58S衍生出的应用面积最大、不育临界温度最低的不育系.但其不育临界温度高于温敏核不育系株1S,杂交制种也没有株1S安全.为了探究培矮64S育性感温的机制,选育不育临界温度更低、杂交制种更安全的不育系,本研究以培矮64S为母本与丰源B杂交,再以杂交后代的不育株与丰源B回交两次制备近等基因系,...     

水稻广亲和性遗传的主基因一多基因混合模型分析

籼、粳亚种间的F1一般表现为半不育,这限制了籼、粳杂种优势的利用。广亲和基因的发现及其遗传研究有助于揭示这种半不育现象的遗传本质,使克服籼、粳亚种间F1的半不育成为可能。本研究采用主基因－多基因混合遗传模型,分析了籼、粳杂交组合3037/02428的P1、P2、F1、B1、B2和F2六世代材料。研究结果显示：广亲和性的遗传除受单个主基因控制外还受多基因的影响。在利用广亲和基因克服亚种间的半不育性时不仅要考虑主基因对育性的作用,也不能忽视多基因对育性的影响。     

籼型光敏核不育水稻育性可转换性的基因定位和基因互作研究

本研究以来源于农垦58S的籼型光敏核不育系培矮64S(短日条件下育性难转换)和8902S(短日条件下育性易转换)及其F１、F２群体为材料,通过短日不同光温和不同生态条件4种处理,利用RFLP分子标记研究了影响光敏核不育水稻在短日条件下的育性可转换性的遗传、基因定位和基因互作,主要结果表明：影响光敏核不育水稻的育性可转换性表现为微效基因的作用,定位了7个控制光敏核不育水稻的育性可转换性QTL,即S2、S3a、S3b、S5、S8和S10。揭示了基因互作真实存在于光敏核不育水稻中,基因互作形式和互作类型对光敏核不育水稻的育性可转换性的影响表现多种多样,不同类型的基因互作所解释的遗传变异处于2.15%～10.07%之间。     

在光氧化条件下不同类型高产稻的叶绿素荧光特性和膜脂过氧化特点

用不同类型高产稻(Oryza sativa L.)粳稻9516、具有粳型成分的两系法亚种间杂交稻培矮64/E32、两优培九(培矮64/9311)和籼型杂交稻X07S/紫恢100、冈优881、汕优63为材料,研究了孕穗期叶片在光氧化条件下的叶绿素荧光特性和膜脂过氧化表现.光氧化处理后,与籼型杂交稻比较,粳稻和具有粳型组分的亚种间杂交稻的PSⅡ原初光化学效率(Fv/Fm)、PSⅡ的线性电子传递的量子效率(ΦPSⅡ)和光化学猝灭系数(qP)下降的较少;超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、过氧化物酶(POD)诱导的活性较高,活性氧 (O(-)/()2、H2O2)和丙二醛(MDA)的产生积累较少,叶绿素和蛋白质含量下降较少,表现出耐光氧化特性,这与在自然条件下生育后期叶绿素含量变化相一致.相关分析表明它们的耐光氧化特性与结实率密切相关,说明耐光氧化品种抗早衰,有利籽粒充实.这些结果启示我们:从超高产育种出发,兼顾杂种优势利用和抗早衰两方面考虑,在母本不育系中引入粳型成分是一个值得重视的育种策略.     

利用初级三体定位水稻光敏核不育基因

自 1 973年 Ramanunjam首次获得三体 ( 2 n=2 x 1 =2 5)植株以来 ,已报道的粳型初级三体有日本晴 NT和籼型初级三体 IR36、Sona、广陆矮 4号 [1 ]及籼型初级三体 30 37[2 ]等。获得细胞学证据并用于定位研究的仅有日本晴三体和 IR36三体 [3,4]。目前 ,利用形态标记和分子标记定位水稻光敏核不育基因的报道较多 ,且涉及到第 5、7和第 1 2三条染色体 [5,6] 。我们拟以粳型光敏核不育系为父本 ,台中 65初级三体为母本配组 ,定位光敏核不育基因 ,对粳型光敏核不育基因定位结果进行验证 ,以期为光敏核不育的利用与研究提供理论依据。1 　材料…     

水稻广亲和性和胞质雄性不育恢复性的遗传分析

对经花培育成的广亲和恢复系ＴＧ７、ＴＧ８的遗传分析表明：ＴＧ７、ＴＧ８均带有１对广亲和基因,与ＣＰＳＬＯ１７、０２４２８的广亲和基因等位。广亲和基因与雄性不育恢复基因表现为独立遗传,野败型（籼）和滇－Ｉ型（粳）不育胞质的育性恢复基因非等位。ＴＧ７和ＴＧ８分别带有２对野败不育胞质和１对滇－Ｉ型不育胞质的恢复基因,分别来自亲本明恢６３和ＣＰＳＬＯ１７。     

水稻光敏核不育系的选育

湖北光敏感核不育水稻的发现,为两系杂交稻奠定了基础。农垦58S为晚梗型,经济性状不理想,直接利用于生产较困难,必须将光敏核不育特性转育到优良的籼、粳品种中,选育出符合生产要求的光敏核不育系,才有生产利用价值。光周期诱导水稻雄性育性转换特性是由1—2对主效基因控制的,可以通过杂交转育。自八十年代以来,湖北和全国的水稻遗传育种学家开展了水稻光敏核不育系的选育,到1991年止,由农垦58S为源的通过省级以上鉴定的水稻光(温)敏核不育系18个,其中籼稻10个粳稻8个,由光、温敏核不育系配制的两系杂交稻组合开始用于生产。     

水稻广亲和性遗传的再研究

水稻广亲和基因的利用是克服亚种间杂种不育性的重要途径。但在广亲和性的遗传上不同研究者的结论不尽一致。以3种有广亲和品种参加的三交组合为研究材料,研究了品种Ketan Nangka的广亲和性遗传。结果表明水稻亚种杂交F1同时存在着雄性不育和雌性不育,但雄性不育对小穗育性的作用大小因组合而异;无论是在雄性不育位点还是雄性不育位点上,Ketan Nangka均具有相对应的中性基因（广亲和基因）;广亲和性的遗传特点与所用的籼粳测验品种间的杂种不育性密切相关;S－5位点的广亲和基因遗传符合单位点孢子体－配子体互作模型。     

Glucocorticoid receptor heterozygosity combined with lack of receptor auto-induction causes glucocorticoid resistance in Jurkat acute lymphoblastic leukemia cells

Glucocorticoids (GC) induce apoptosis in malignant lymphoblasts, but the mechanism of this process as well as that of the clinically important GC resistance is unknown. We investigated GC resistance in Jurkat T-ALL cells in which ectopic GC receptor (GR) restores GC sensitivity, suggesting deficient GR expression. Jurkat cells expressed one wild-type and one mutated (R477H) GR allele. GR(R477H) ligand-binding-dependent nuclear import, as revealed by live-cell microscopy of YFP-tagged GR, was unaffected. Transactivation and transrepression were markedly impaired; however, GR(R477H) did not act in a dominant-negative manner, that is, did not prevent cell death, when introduced into a GC-sensitive cell line by retroviral gene transfer. Contrary to another GR heterozygous, but GC-sensitive, T-ALL model (CCRF-CEM), Jurkats expressed lower basal GR levels and did not auto-induce their GR, as revealed by 'real-time' RT-PCR and immunoblotting. Absent GR auto-induction could not be restored by transgenic GR and, hence, was not caused by reduced basal GR levels. Thus, inactivation of one GR gene results in haploinsufficiency if associated with lack of GR auto-induction.     

Transrepression function of the glucocorticoid receptor regulates eyelid development and keratinocyte proliferation but is not sufficient to prevent skin chronic inflammation

Glucocorticoids (GCs) play a key role in skin homeostasis and stress responses acting through the GC receptor (GR), which modulates gene expression by DNA binding-dependent (transactivation) and -independent (transrepression) mechanisms. To delineate which mechanisms underlie the beneficial and adverse effects mediated by GR in epidermis and other epithelia, we have generated transgenic mice that express a mutant GR (P493R, A494S), which is defective for transactivation but retains transrepression activity, under control of the keratin 5 promoter (K5-GR-TR mice). K5-GR-TR embryos exhibited eyelid opening at birth and corneal defects that resulted in corneal opacity in the adulthood. Transgenic embryos developed normal skin, although epidermal atrophy and focal alopecia was detected in adult mice. GR-mediated transrepression was sufficient to inhibit keratinocyte proliferation induced by acute and chronic phorbol 12-myristate 13-acetate exposure, as demonstrated by morphometric analyses, bromodeoxyuridine incorporation, and repression of keratin 6, a marker of hyperproliferative epidermis. These antiproliferative effects were mediated through negative interference of GR with MAPK/activator protein-1 and nuclear factor-kappaB activities, although these interactions occurred with different kinetics. However, phorbol 12-myristate 13-acetate-induced inflammation was only partially inhibited by GR-TR, which efficiently repressed IL-1beta and MMP-3 genes while weakly repressing IL-6 and TNF-alpha. Our data highlight the relevance of deciphering the mechanisms underlying GR actions on epithelial morphogenesis as well as for its therapeutic use to identify more restricted targets of GC administration.     

秋稻品种Dular广亲和基因的RFLP分析

利用Ｂａｌｉｌｌａ／Ｄｕｌａｒ／ＩＲ３６和南京１１／／Ｄｕｌｕｒ／２５３３两个三交Ｆ１ 本对秋稻品种Ｄｕｌａｒ的广亲和性进行了遗传分析。为使杂种群体在相对一致的条伯下抽穗,所有三交Ｆ１植株于分化前集中进行了为期１周的短日照处理。结果表明,两个群体的小穗育性于多峰连续分布,说明三交群体的育性可能受几个主基因控制并受到微效基因的修饰,进一步采用分群分析法,以南京１１／／Ｄｕｌａｒ／２５３３为分析群体进     

Non-genomic events determining the sensitivity of hemopoietic malignancies to glucocorticoid-induced apoptosis

Glucocorticoid (GC) hormones have been introduced as therapeutic agents in blood cancers six decades ago. The effectiveness of GC treatment stems from its ability to induce apoptotic death of hemopoietic cells. A major impediment in GC therapy is the acquisition of resistance to the drug upon repeated treatment. In addition, some blood cancers are a priori resistant to GC therapy. Usually, resistance to GC correlates with poor prognosis. Albeit the wide use of GC in clinical practice, their mode of action is not fully understood. The cellular response to GC is initiated by its binding to the cytosolic GC receptor (GR) that translocates to the nucleus and modulates gene expression. However, nuclear activities of GR occur in both apoptosis-sensitive and apoptosis-resistant cells. These apparent controversies can be resolved by deciphering non-genomic effects of GCs and the mode by which they modulate the apoptotic response. We suggest that non-genomic consequences of GC stimulation determine the cell fate toward survival or death. Understanding the cellular mechanisms of GC apoptotic sensitivity contributes to the development of new modalities for overcoming GC resistance.