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1.
小麦品种苏麦3号抗赤霉病基因的染色体定位研究   总被引:11,自引:3,他引:11  
本研究以苏麦3号为染色体供体,一套“中国春”小麦单体系列分别作为受体和轮回母本,连续回交4次,并建立两套独立转育的重复系,对赤霉病抗性进行了染色体定位研究。结果表明,重复系Ⅰ中,苏麦3号染色体2B、3B和6B与赤霉病抗性有关;重复系Ⅱ中,染色体7A、2B、3B和6B与赤霉病抗性有关。由此推断,苏麦3号的抗性基因位于染色体2B、3B和6B上,染色体7A是否具有抗性基因,还有待于进一步证实。2D染色体载有促进赤霉病扩展的感病基因。  相似文献   

2.
小麦赤霉病是由禾谷镰孢菌引起的一种世界性重要病害,严重威胁小麦生产安全。黄淮麦区作为我国小麦主产区,赤霉病危害日趋严重,因缺乏半冬性抗源,抗赤霉病育种进展缓慢。Fhb1基因是迄今发现的效应最大、抗性最稳定,也是被广泛应用于全球小麦赤霉病抗性育种的主效基因,但Fhb1基因在黄淮麦区尚未被广泛应用。本研究以感病品种矮抗58为轮回亲本, H35为Fhb1基因供体亲本,通过有限回交和分子标记辅助选择,同时利用双单倍体育种和传统系谱选育两种方法,培育出了一批综合性状较好、具有Fhb1基因的优良新品系,其中徐麦DH9和徐麦17252经多年鉴定均达到中抗水平。在以徐麦36和徐麦2023为杂交父本的后代品系中,含Fhb1基因的家系赤霉病平均抗性明显优于感病对照。Fhb1基因的导入显著提高了赤霉病抗性,但部分家系对赤霉病仍旧表现出高感水平,说明赤霉病抗性还受到Fhb1基因以外其他遗传因素的显著影响。本研究为Fhb1基因在黄淮麦区抗赤霉病小麦育种中的应用提供了成功的经验。  相似文献   

3.
赤霉病已上升为黄淮冬麦区的主要病害, 提高小麦品种对赤霉病的抗性成为该麦区主要的育种目标之一。宁麦9号、生选6号、建阳798、建阳84、苏麦3号和宁麦13均携带Fhb1基因, 对赤霉病表现中抗水平以上。本研究以这6个品种(系)为供体, 分别与高感赤霉病的周麦16矮败小麦近等基因系杂交和回交, 构建6个回交群体。利用Fhb1基因的KASP标记在回交后代中进行基因型分析, 分别选择携带和不携带Fhb1基因的可育株, 对后代株系进行单花滴注接种鉴定和田间病圃自然鉴定。回交后代携带Fhb1家系整体抗性达到中感, 比不携带Fhb1家系的平均病小穗数低4.2 (P < 0.01), 平均病情指数低4.0, 比轮回亲本周麦16的平均病小穗数和病情指数分别低8.1 (P < 0.01)和28.4 (P < 0.01)。不同供体品种(系)回交后代在赤霉病抗性上表现出明显差异, 以生选6号为供体的回交后代家系抗性表现最好。本研究表明, 利用Fhb1基因分子标记辅助选择技术能够有效地提高黄淮冬麦区小麦品种的赤霉病抗性水平。  相似文献   

4.
小麦品种扬麦16赤霉病抗扩展QTL定位及分析   总被引:1,自引:0,他引:1  
扬麦系列品种赤霉病抗性在世界范围内得到重视,但其抗性遗传机制尚不清楚。扬麦16是近年来大面积推广的抗赤霉病品种,本研究以扬麦16与中麦895杂交构建的174个双单倍体(double haploid lines,DH)系为材料,于2017—2019年连续3年对该群体采用单花滴注进行赤霉病抗扩展鉴定。利用660K SNP芯片构建高密度遗传图谱,共检测到6个抗性QTL,分别位于2DL、3BL、4BS、4DS、5BL和6AS染色体上。除4BS位点外,其他5个抗性等位基因均来源于扬麦16。QFhb.yaas-4DS和QFhb.yaas-6AS均在多年被检测到,可解释8.8%~15.0%的表型变异;QFhb.yaas-2DL、QFhb.yaas-3BL仅在1年被检测到,分别解释10.5%和14.7%的表型变异;QFhb.yaas-5BL和来源于中麦895的QFhb.yaas-4BS仅在1年被检测到且效应仅为6.4%和8.3%。QTL效应分析结果表明,相较于单个位点,多个抗性QTL的聚合可显著降低赤霉病严重度。扬麦16抗赤霉病QTL将为揭示扬麦品种抗性遗传机制及开发相应分子标记奠定基础。  相似文献   

5.
利用"永久F2"群体定位抗赤霉病QTL   总被引:1,自引:0,他引:1  
为了研究抗赤霉病侵染性的遗传, 利用感赤霉病品种南大2419和抗赤霉病品种望水白杂交单粒传获得的重组自交系群体132个株系间的随机配对组合, 构建了一个包含198个株系的“永久 F2”群体。通过两年抗侵染田间试验和QTL作图, 定位了6个抗侵染QTL, 其中抗性等位位点源于望水白的Qfhi.nau-4B和Qfhi.nau-5A以及源于南大2419的Qfhi.nau-2B的效应较为稳定。Qfhi.nau-4B和 Qfhi.nau-5A的效应较大且以加性效应为主, 前者存在部分显性基因效应。此外, 还检测到4对显著的互作位点。这些结果进一步说明赤霉病抗性遗传的复杂性, 同时也表明在利用望水白进行抗赤霉病育种时早代选择抗侵染性是可行的。  相似文献   

6.
小麦赤霉病是一种严重危害小麦生产的真菌性病害,其抗性由多基因控制,抗性机制复杂。type Ⅰ(抗侵入)和type Ⅱ(抗扩展)是小麦抵御赤霉病侵害的2种最主要抗性类型。在抗赤霉病育种中兼顾2种抗性,对于保证生产上抗性的稳定和持久有着重要意义。在前期研究中,作者所在课题组从小麦地方品种望水白中克隆了抗赤霉病扩展的主效QTL Fhb1,精细定位了Fhb4和Fhb5,获得了功能性/紧密连锁的分子标记。本研究利用这些标记,以小麦品系NMAS022作为供体亲本,现代小麦品种百农4199作为受体亲本,通过分子标记辅助回交育种方法选育成了聚合望水白Fhb1、Fhb4、Fhb5的小麦新品系百农4299。与百农4199相比,百农4299在2年的田间试验中type Ⅰ抗性至少增加了73%~74%, type Ⅱ抗性至少增加了83%~88%(以病小穗数计),并且产量潜力也得到了提高。上述结果证明了通过分子标记辅助选择聚合不同类型抗赤霉病QTL以提高小麦赤霉病抗性的可行性。抗赤霉病小麦品系百农4299有望成为一个新的抗赤霉病小麦品种。  相似文献   

7.
小麦赤霉病抗性QTL分析   总被引:13,自引:1,他引:13  
以小麦赤霉病抗源望水白与感病品种Alondra杂交产生的104个重组自交系为材料,采用JoinMap®3.0软件构建了含有2个RAPD、109个SSR和105个AFLP标记共25个连锁群的遗传连锁图,其中24个连锁群可以确定为相应的染色体;采用自然发病和土表接种方法,对该重组自交系群体在建阳和苏州进行了连续两年赤霉病抗性鉴定,结果表明:  相似文献   

8.
为了研究抗赤霉病侵染性的遗传, 利用感赤霉病品种南大2419和抗赤霉病品种望水白杂交单粒传获得的重组自交系群体132个株系间的随机配对组合, 构建了一个包含198个株系的“永久F2”群体。通过两年抗侵染田间试验和QTL作图, 定位了6个抗侵染QTL, 其中抗性等位位点源于望水白的Qfhi.nau-4B和Qfhi.nau-5A以及源于南大2419的Qfhi.nau-2B的效应较为稳定。Qfhi.nau-4B和Qfhi.nau-5A的效应较大且以加性效应为主, 前者存在部分显性基因效应。此外, 还检测到4对显著的互作位点。这些结果进一步说明赤霉病抗性遗传的复杂性, 同时也表明在利用望水白进行抗赤霉病育种时早代选择抗侵染性是可行的。  相似文献   

9.
利用DH群体动态检测水稻抗褐飞虱数量性状基因位点   总被引:9,自引:0,他引:9  
利用籼粳交珍汕97/武育粳2号F1花培获得的190个双单倍体群体(doubled—haploid population,DH系)及其构建的179个SSR分子标记遗传图谱,通过对DH系群体苗期重复接虫试验和2个不同时期对褐飞虱危害程度进行动态调查,并应用Mapmaker/exp Version3.0和Windows QTL Cartographer V2.0对水稻抗褐飞虱数量性状基因位点(quantative trait locus,QTL)进行动态检测和遗传效应分析。结果表明,在苗期对褐飞虱抗性的检测中,共检测到6个抗性QTL,分别位于第2、3、4、8和10染色体上,各QTL的LOD值分别为2.22-4.64,贡献率为5.04%~13.73%,第3染色体和第4染色体上各有1个OTL的加性效应为正值,表明来自于亲本武育粳2号的这2个位点的等位基因可以提高水稻对褐飞虱的抗性,其余4个QTL的加性效应均为负值,表明来自于亲本珍汕97的这些位点的等位基因可以提高水稻对褐飞虱的抗性。  相似文献   

10.
利用农杆菌介导法将几丁质酶基因和b-1,3-葡聚糖酶双价基因导入小麦品种扬麦10号和Bobwhite,共得到了13棵T0代转基因植株,2个小麦品种的转化效率分别为1.4%和1.0%。T1代植株赤霉病抗性鉴定结果表明,转基因植株对赤霉病具有一定抗性,小穗发病率4.76%~11.76%,低于抗病对照和感病对照。T1代植株分子检测结果表明,外源基  相似文献   

11.
抗赤霉病小麦新品种扬麦18的选育研究   总被引:3,自引:2,他引:1  
小麦赤霉病是世界范围灾害性小麦病害。为了培育和推广抗赤霉病小麦品种,解决赤霉病对长江中下游地区小麦生产的危害。通过高产育种和抗赤霉病育种技术路线有机结合,运用“综合性状协调点”的观点,培育出了综合性状优良,多年表现既高产稳产又抗赤霉病(MR-R)小麦品种扬麦18,在生产上大面积推广应用。该品种的育成与推广应用初步实现了小麦抗赤霉病育种目标。  相似文献   

12.
Summary Fusarium head blight (FHB) is a serious disease of wheat worldwide that may cause substantial yield and quality losses. Breeding for FHB-resistant cultivars is the most cost-effective approach to control FHB. The objective of the present study was to determine the relationship of resistance between new resistant sources and Sumai 3 using five simple sequence repeat (SSR) markers closely linked to the major QTL for FHB resistance on chromosome arms 3BS and 6BS. All five SSR markers were highly polymorphic between Sumai 3 (and its derivatives) and susceptible Canadian wheat lines. Most of the Sumai 3-derived Chinese wheat accessions and three Canadian FHB-resistant lines had all the Sumai 3 SSR marker alleles on chromosome arms 3BS and 6BS. The Chinese landrace Wangshuibai and two Japanese accessions Nobeokabozu and Nyu Bai had the same banding patterns as Sumai 3 for all five SSR marker alleles, and another Chinese landrace Fangshanmai had three of the five SSR markers in common with Sumai 3, and therefore most likely carries the same QTL as Sumai 3 on 3BS and 6BS. The Brazilian cultivar Frontana had no alleles in common with Sumai 3 on either QTL, and the Chinese landrace Hongheshang had only one of the five SSR markers in common with Sumai 3, therefore likely carrying resistance genes different from Sumai 3. The Italian cultivar Funo is not the donor of either the 3BS QTL or 6BS QTL. All five SSR seem to be effective candidates for marker-assisted selection to increase the level of resistance to FHB in wheat breeding programs.  相似文献   

13.
以禾谷镰刀菌(Fusarium graminearum Schwabe)菌株进行穗部喷雾和单花滴注接种,评价了10个小麦抗源的赤霉病和脱氧雪腐镰刀菌烯醇(DON)积累抗性。结果表明,望水白、苏麦3号、延岗坊主、繁60096属于高抗品种,Frontana表现感病,其余品种表现中抗。除Frontata外,所有抗源DON含量在3 mg/kg以下。不同接种方法间、不同致病菌株间的病小穗率和DON含量以及同一处理内的病小穗率和DON含量间呈极显著相关。利用与已报道的赤霉病抗性QTL相关SSR引物对供试材料进行PCR扩增,比较扩增产物等位位点的差异,除4B染色体的GWM113标记外,其余标记在品种间具有2~8个等位位点,多态信息含量为0.14~0.85。单倍型分析表明,延岗坊主具有与望水白一致的3B主效QTL的SSR标记位点,扬麦158和新中长分别在2D和4B上具有多个与武汉1号一致的抗性QTL相关SSR位点,翻山小麦在3B和6B上具有多个与苏麦3号或望水白一致的抗性QTL相关SSR位点,繁60096在2D上有多个与武汉1号一致的QTL相关SSR标记,而镇麦7459和温州红和尚与已报道的小麦赤霉病抗性多数SSR位点不一致,可能具有不同的抗性基因。  相似文献   

14.
Fusarium head blight (FHB) is an important disease of wheat (Triticum aestivum L.). The aim of this study was to determine the effects of quantitative trait locus (QTL) regions for resistance to FHB and estimate their effects on reducing FHB damage to wheat in Hokkaido, northern Japan. We examined 233 F1-derived doubled-haploid (DH) lines from a cross between ‘Kukeiharu 14’ and ‘Sumai 3’ to determine their reaction to FHB during two seasons under field conditions. The DH lines were genotyped at five known FHB-resistance QTL regions (on chromosomes 3BS, 5AS, 6BS, 2DL and 4BS) by using SSR markers. ‘Sumai 3’ alleles at the QTLs at 3BS and 5AS effectively reduced FHB damage in the environment of Hokkaido, indicating that these QTLs will be useful for breeding spring wheat cultivars suitable for Hokkaido. Some of the QTL regions influenced agronomic traits: ‘Sumai 3’ alleles at the 4BS and 5AS QTLs significantly increased stem length and spike length, that at the 2DL QTL significantly decreased grain weight, and that at the 6BS QTL significantly delayed heading, indicating pleiotropic or linkage effects between these agronomic traits and FHB resistance.  相似文献   

15.
Fusarium head blight (FHB) poses a challenge for wheat breeders worldwide; there are limited sources of resistance and the genetic basis for resistance is not well understood. In the mid-1980s, a shuttle breeding and germplasm exchange program launched between CIMMYT-Mexico and China, enabled the incorporation of FHB resistance from Chinese bread wheat germplasm into CIMMYT wheat. Most of the Chinese wheat materials conserved in the CIMMYT germplasm bank had not been fully characterized for FHB reaction under Mexican environments, until 2009, when 491 Chinese bread wheat lines were evaluated in a FHB screening nursery in Mexico, and 304 (61.9 %) showed FHB indices below 10 %. Subsequent testing occurred in 2010 for plant height (PH), days to heading (DH), and leaf rust response. In 2012, 140 elite lines with good agronomic types were further evaluated for field FHB reaction and deoxynivalenol (DON) accumulation. Most of the tested lines showed good resistance: 116 (82.9 %) entries displayed FHB indices lower than 10 %, while 89 (63.6 %) had DON contents lower than 1.0 ppm. Significant negative correlations were observed between FHB traits (FHB index, DON content, and Fusarium damaged kernels) and PH, DH, and anther extrusion. A subset of 102 elite entries was selected for haplotyping using markers linked to 10 well known FHB quantitative trait loci (QTL). 57 % of the lines possessed the same 2DL QTL marker alleles as Wuhan 1 or CJ 9306, and 26.5 % had the same 3BS QTL allele as Sumai 3. The remaining known QTL were of low frequency. These materials, especially those with none of the above tested resistance QTL (26.5 %), could be used in breeding programs as new resistance sources possessing novel genes for FHB resistance and DON tolerance.  相似文献   

16.
Summary A doubled haploid (DH) wheat population derived from the cross Wangshuibai/Alondra‘s’ was developed through chromosome doubling of haploids generated by anther culture of hybrids. Fusarium head blight (FHB) was evaluated for three years from 2001 to 2003 in Jianyang, Fujian Province, China, where epidemics of FHB have been consistently severe. After 307 pairs of simple sequence repeat (SSR) primers were screened, 110 pairs were polymorphic between Wangshuibai and Alondra`s’, and used to construct a genetic linkage map for detection of quantitative trait loci (QTLs). A stable QTL for low FHB severity was detected on chromosomes 3B over all three years, and QTLs on chromosomes 5B, 2D, and 7A were detected over two years. Additional QTLs on chromosomes 3A, 3D, 4B, 5A, 5D, 6B and 7B showed marginal significance in only one year. Six QTLs were detected when phenotypic data from three years were combined. In addition, significant additive-by-additive epistasis was detected for a QTL on 6A although its additive effect was not significant. Additive effects (A) and additive-by-additive epistasis (AA) explained a major portion of the phenotypic variation (76.5%) for FHB response. Xgwm533-3B and Xgwm335-5B were the closest markers to QTLs, and have potential to be used as selectable markers for marker-assisted selection (MAS) in wheat breeding programs.  相似文献   

17.
由镰孢属(Fusarium)真菌侵染引起的赤霉病是严重威胁小麦生产的重要病害之一,但小麦育种中可直接利用的抗源非常有限。采用单花滴注法接种赤霉菌株F0609,对来源于中间偃麦草或长穗偃麦草的119份小偃麦衍生品系进行3年6个环境的抗病鉴定,发现平均病小穗率<10%的材料有13份,抗性评价为抗病(R);平均病小穗率介于10%~25%之间的材料有61份,抗性评价为中抗(MR);其余45份材料的平均病小穗率介于25%~50%或>50%,抗性评价为中感或高感(MS和S)。在13份高抗赤霉病材料中,CH16387的抗性显著优于苏麦3号和望水白,CH16371和CH16379的抗性显著优于望水白,其余10个品系与抗病对照苏麦3号和望水白的抗性水平相当。这13份材料分别来自小麦-中间偃麦草部分双二倍体TAI8045和小麦-长穗偃麦草部分双二倍体TAP8430与普通小麦的杂交组合,TAI8045抗性显著优于对照品种望水白, TAP8430与苏麦3号和望水白的抗性相当,而杂交组合中的小麦亲本对赤霉病表现感病,推测这些材料的抗性可能来自TAI8045和TAP8430。这些抗病材料为小麦抗赤霉病育种提供了新的种质资源。  相似文献   

18.
小麦品种赤霉病抗性的遗传研究   总被引:3,自引:0,他引:3  
利用8个不同抗性小麦品种双列杂交的F1及其亲本,以赤霉病病粒率为抗性指标,研究了小麦赤霉病抗性的遗传。结果表明,参试品种间存在3~4对赤霉病抗性基因的差异,苏麦3号、宁麦9号和扬麦158具有较多控制赤霉病抗性遗传的显性基因,对于减少它们杂交后代的病粒率有较高的一般配合力。小麦赤霉病抗性符合加性-显性模型。赤霉  相似文献   

19.
The genetic constitution of resistance to Fusarium head blight (FHB, scab) caused by Fusarium graminearum in the Chinese wheat cultivar Sumai 3 and the Japanese cultivar Saikai 165 was investigated using doubled haploid lines (DHLs) and recombinant inbred lines (RILs). Frequency distributions of DHLs derived from two F1 crosses, Sumai 3 (very resistant to resistant; VR-R) / Gamenya (very susceptible; VS) and Sumai 3 / Emblem (VS), fitted well to 1: 2: 1 (resistant: moderately resistant: susceptible) ratios for reaction to FHB in the field. It is suggested that the resistance of Sumai 3 is controlled by two major genes with additive effects. One of the resistance genes may be linked in repulsion to the dominant suppressor B1 for awnedness with recombination values 15.1 ± 3.3% in Sumai 3 /Gamenya and 21.4 ± 4.3% in Sumai 3 / Emblem. Saikai 165 is a Japanese resistant line derived from an F1 Sumai 3 / Asakaze-komugi (moderately resistant; MR). The data for RILs derived from the cross Emblem / Saikai 165, indicates that three resistance genes control the resistance of Saikai 165. This revised version was published online in July 2006 with corrections to the Cover Date.  相似文献   

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