黑腹果蝇3号染色体裂翅平衡致死位点的发现及2号、3号染色体裂卷翅双平衡染色体的建立

果蝇的平衡染色体在遗传研究中被广泛应用.文章通过分析黑腹果蝇裂翅新突变体与野生型、982紫眼及黑檀体杂交后代裂翅性状情况,首次将裂翅基因定位于3号染色体上,并阐明了裂翅平衡致死、杂合子纯繁的遗传机制,获得了以裂翅为显性标记的3号平衡染色体品系.探索了双平衡染色体显性标记基因聚合的杂交模式,成功建立了以裂翅和卷翅为标记的2号、3号双平衡染色体.裂翅的发现为3号染色体平衡子提供了更加方便识另0的显性翅型标记,同时裂卷翅双平衡体的建立丰富了果蝇常用工具平衡子,可以广泛用于基因定位及突变筛选过程.     

黑腹果蝇white基因在H_2O_2影响下卷翅形成中的作用及机理

卷翅是果蝇遗传学上最常用的标记之一,但卷翅形成的具体机制还不清楚.过去的研究发现,理化刺激影响果蝇卷翅的形成.我们最近研究发现,H_2O_2处理不仅会影响果蝇的羽化率,还会使其出现卷翅现象.本研究通过改变H_2O_2浓度、果蝇培养温度和H_2O_2处理时间,探讨影响黑腹果蝇卷翅形成的具体因素,并对其超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-PX)活力进行检测,探讨H_2O_2对果蝇抗氧化能力的影响.结果表明:果蝇的羽化率与H_2O_2浓度成反比.温度、H_2O_2浓度和H_2O_2处理时间的改变均会影响果蝇翅的卷曲程度和卷翅果蝇所占的比例.其中white基因突变果蝇对这3种条件反应最明显,mini-white(white基因回复突变)果蝇却可以拯救该表型,它的反应与野生型OR相似.H_2O_2对含Cy基因的果蝇卷翅的形成也有一定的影响,可以加大果蝇翅的卷曲程度.对SOD、CAT和GSH-PX活力检测发现,H_2O_2处理会使果蝇的抗氧化能力降低.实时荧光定量PCR检测发现,H_2O_2处理会导致果蝇基因表达量发生改变.黑腹果蝇卷翅形成是一个十分复杂的过程,H_2O_2可能作为某种信号分子或是间接影响某种因子参与黑腹果蝇的卷翅形成过程.该卷翅形成过程可能与Cy基因导致的果蝇卷翅过程是同一个信号途径,两者也可能是通过不同的模式进行调控的.     

黑腹果蝇white基因在H2O2影响下卷翅形成中的作用及机理

卷翅是果蝇遗传学上最常用的标记之一,但卷翅形成的具体机制还不清楚.过去的研究发现,理化刺激影响果蝇卷翅的形成.我们最近研究发现,H₂O₂处理不仅会影响果蝇的羽化率,还会使其出现卷翅现象.本研究通过改变H₂O₂浓度、果蝇培养温度和H₂O₂处理时间,探讨影响黑腹果蝇卷翅形成的具体因素,并对其超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-PX)活力进行检测,探讨H₂O₂对果蝇抗氧化能力的影响.结果表明: 果蝇的羽化率与H₂O₂浓度成反比.温度、H₂O₂浓度和H₂O₂处理时间的改变均会影响果蝇翅的卷曲程度和卷翅果蝇所占的比例.其中white基因突变果蝇对这3种条件反应最明显,mini-white(white基因回复突变)果蝇却可以拯救该表型,它的反应与野生型OR相似.H₂O₂对含Cy基因的果蝇卷翅的形成也有一定的影响,可以加大果蝇翅的卷曲程度.对SOD、CAT和GSH-PX活力检测发现,H₂O₂处理会使果蝇的抗氧化能力降低.实时荧光定量PCR检测发现,H₂O₂处理会导致果蝇基因表达量发生改变.黑腹果蝇卷翅形成是一个十分复杂的过程,H₂O₂可能作为某种信号分子或是间接影响某种因子参与黑腹果蝇的卷翅形成过程.该卷翅形成过程可能与Cy基因导致的果蝇卷翅过程是同一个信号途径,两者也可能是通过不同的模式进行调控的.     

红松长翅卷蛾——中国新记录种

红松长翅卷蛾Acleris kodamai系T.Yasuda根据在日本采到的一只不完整的雄蛾标本记述的。笔者1984～1986年9～11月在辽宁省东沟县采集、饲养,获得大量卷蛾标本,经鉴定,为红松长翅卷蛾,这是该种在我国的首次记录。现将雌性外生殖器与不同斑纹补充记述如下。     

单、双因子杂种交配的模拟试验

（一）甚本原理 果蝇的单、双因子实验Ill可用计算机模拟。假定 模拟的第一个性状是翅形,由第二染色体上的V-。位 点（假定为第一位点）控制,长翅(V）对残翅(v)是 显性;第二个性状是体色,由第三染色体上的E-。位 点（第二位点）控制,灰体（幻对黑檀体（。）是显性。     

家蚕BmRpt4基因在翅膀发育中的功能研究

【目的】研究分析编码蛋白酶体调控复合物亚基基因BmRpt4(Regulatoryparticletriple-A ATPase4,BGIBMGA010794)在家蚕翅膀发育过程中的功能。【方法】利用CRISPR/Cas9基因组编辑技术,将BmRpt4的gRNAs和Cas9mRNA直接注射到家蚕胚胎中,观察G0代家蚕个体雏翅率,并分析雏翅个体中BmRpt4基因突变情况。【结果】经统计,对照组G0代家蚕个体均表现为正常翅,而实验组注射BmRpt4的gRNAs和Cas9 mRNA后,G0代约66.7%家蚕个体表现出小翅表型。在分子水平上对小翅表型个体进行检测,发现BmRpt4基因在两个gRNA及其之间位置均有不同长度片段的缺失或者插入,说明在这些突变个体中BmRpt4基因被不同程度的敲除,从而其功能缺失,导致出现小翅表型。【结论】该研究结果表明编码蛋白酶体调控亚基的BmRpt4基因在家蚕翅膀发育中具有重要作用,为蛋白酶体在生物组织器官发育中调控作用研究提供重要实验依据。     

葡萄花翅小卷蛾抗药性研究进展

葡萄花翅小卷蛾是葡萄上的重要害虫,具有多食性、多化性等生物学特点,抗逆能力极强。该虫起源于欧洲,现已入侵全球多个国家。葡萄花翅小卷蛾主要以幼虫取食葡萄花序、幼果和成熟果实,给葡萄生产造成重大损失;其危害有利于真菌的侵入,导致灰霉病、白粉病等病害大量发生,从而造成葡萄腐烂。由于该虫入侵风险极高,已被我国列为重要的进境检疫性有害生物。国外对葡萄花翅小卷蛾的防治主要采用化学杀虫剂,由于长期大量且不合理地使用化学杀虫剂,葡萄花翅小卷蛾已对多种不同类型的杀虫剂产生了抗药性。本研究总结了葡萄花翅小卷蛾的抗性测定方法、抗性现状及其抗性机理,同时结合国外葡萄花翅小卷蛾抗性和防治相关研究,提出该虫抗性治理策略,并对我国预防该虫的入侵提出建议。     

世界性害虫葡萄花翅小卷蛾入侵我国的风险分析

【目的】葡萄花翅小卷蛾是我国禁止进境的检疫性害虫,一旦入侵我国,将会给葡萄产业和林果业造成严重损失。开展葡萄花翅小卷蛾入侵我国的风险分析可为该虫的检疫和预警提供依据。【方法】介绍了葡萄花翅小卷蛾的形态特征和生物学特性,并参照通用的有害生物风险评估方法,从该虫在国内外的发生情况、潜在的经济危害性、受害作物的经济重要性、传播扩散的可能性及风险管理的难度等方面,对其入侵风险进行了定性和定量分析。【结果】葡萄花翅小卷蛾是一种对我国有很大潜在威胁的有害生物,其风险值为2.14,属高度危险性有害生物。【结论】建议新疆等口岸比较多的省、自治区口岸检疫部门加强对该害虫的检疫力度,杜绝其传入我国。     

不同染色技术和双色荧光原位杂交技术对宽翅菘蓝 （Isatis violascens Bunge）的细胞遗传学分析

为了解十字花科菘蓝属植物宽翅菘蓝(宽翅菘蓝,Isatis violascens Bunge)的染色体结构,本文利用45SrDNA和5SrDNA双色荧光原位杂交、银染技术和CMA3对宽翅菘蓝进行分子细胞遗传学研究。45SrDNA和5SrDNA荧光原位杂交结果显示宽翅菘蓝染色体上有1对45SrDNA信号和1对5SrDNA信号;银染结果显示其中期染色体有1对银染点;CMA3染色结果发现宽翅菘蓝中期染色体存在1对CMA3信号。     

不同染色技术和双色荧光原位杂交技术对宽翅菘蓝（Isatis violascens Bunge）的细胞遗传学分析

为了解十字花科菘蓝属植物宽翅菘蓝（宽翅菘蓝,Isatis violascens Bunge）的染色体结构,本文利用45SrDNA和5SrDNA双色荧光原位杂交、银染技术和CMA3对宽翅菘蓝进行分子细胞遗传学研究。45SrDNA和5SrDNA荧光原位杂交结果显示宽翅菘蓝染色体上有1对45SrDNA信号和1对5SrDNA信号;银染结果显示其中期染色体有1对银染点;CMA3染色结果发现宽翅菘蓝中期染色体存在1对CMA3信号。     

Mechanism of the fluorescent light induced suppression of Curly phenotype in Drosophila melanogaster

A dominant mutation Curly (Cy), frequently used as a marker on the second chromosome in Drosophila melanogaster, was previously shown to be suppressed by several factors, including larval crowding, low temperature, and fluorescent light. While the first two factors affect this mutation only partially, fluorescent tube exposed flies exhibit an almost completely suppressed (wild type) phenotype. This suppressive effect is the result of a combination of the electric field and light, both factors being produced by common fluorescent tubes. In this study, experiments were carried out to clarify the basic mechanism of this unique phenomenon. Two fluorescent tube sensitive stages of Drosophila development were found in the second half of embryonic development and first half of the pupal stage. Riboflavin, which is administered to Drosophila larvae with yeast, and decomposed by light, seems to play a key role in this phenomenon. In a medium lacking riboflavin caused by light exposure, Cy expression is inhibited by the action of electric field. Positive results of experiments with lithium ions, which block the opening of Ca(2+) channels, support the hypothesis that electromagnetic fields may alter ion currents during ontogenic development of Drosophila, and thus influence, expression of the Cy gene. Also, fluorescent light induces an overexpression of a specific protein in the imaginal wing disc of Cy pupae.     

Molecular characterization of the afl-1 locus in Aspergillus flavus.

An unusual mutation at the afl-1 locus, affecting aflatoxin biosynthesis in Aspergillus flavus 649, was investigated. The inability of strain 649 to produce aflatoxin was found to be the result of a large (greater than 60 kb) deletion that included a cluster of aflatoxin biosynthesis genes. Diploids formed by parasexual crosses between strain 649 and the aflatoxigenic strain 86 did not produce aflatoxin, indicating the dominant nature of the afl-1 mutation in strain 649. In metabolite feeding experiments, the diploids did not convert three intermediates in the aflatoxin pathway to aflatoxin. Northern (RNA blot) analysis of the diploids grown in medium conducive for aflatoxin production indicated that the aflatoxin pathway genes nor1, ver1, and omt1 were not expressed; however, there was low-level expression of the regulatory gene aflR. Pulsed-field electrophoresis gels indicated a larger (6 Mb) chromosome in strain 649 than the apparently homologous (4.9 Mb) chromosome in strain 86. The larger chromosome in strain 649 suggests that a rearrangement occurred in addition to the deletion. From these data, we proposed that a trans-sensing mechanism in diploids is responsible for the dominant phenotype associated with the afl-1 locus in strain 649. Such a mechanism is known in Drosophila melanogaster but has not been described for fungi.     

Ectopic Expression of the Drosophila Homeotic Gene Proboscipedia under Antennapedia P1 Control Causes Dominant Thoracic Defects

A deletion mutation in the Antennapedia Complex of Drosophila melanogaster, Df(3R)SCBXL2, induces both dominant and recessive loss-of-function phenotypes. The deletion is associated with diminished function of proboscipedia (pb), a homeotic gene required for mouthparts formation. Df(3R)SCBXL2 also has associated dominant thoracic defects related to diminished expression of the homeotic Antennapedia (Antp) gene copy on the homologous chromosome. This is shown to be a consequence of ectopic pb expression in the thorax. Newly juxtaposed Antp sequences provide the pb gene on the deletion bearing chromosome with a second promoter, Antp P1, in addition to its own. Ectopic pb protein expression occurs under Antp P1 control, by alternate splicing, and results in diminished accumulation of Antp protein in the imaginal disc cells where Antp P1 is normally expressed. The analysis of this mutant chromosome thus demonstrates that pb protein is capable of participating in the negative regulation of a more posteriorly expressed homeotic gene, as well as serving a homeotic "selector" function in the head.     

Repairs of X-ray induced sublethal damage in class B oocytes of Drosophila melanogaster.

Repair of X-ray-induced sublethal damage (Elkind-type recovery) in class B oocytes of Drosophila melanogaster was studied. Newly hatched females of two different stocks were treated with either acute or fractionated exposures. For the fractionation experiments a constant time interval of one hour between the dose fractions was used. As genetic endpoints dominant lethality, chromosome aberrations (detachments) and non-disjunction were studied. The repair of X-ray-induced sublethal damage in class B oocytes is expressed as a reappearance on the initial shoulder in the fractionation curve. For dominant lethality it could be shown that less sublethal damage is repaired in oocytes of Berlin wild females than in those of attached-X females (on the average 76 per cent and 101 per cent respectively). Complete repair (about 100 per cent) was observed for detachments in occytes of attached-X females. Within the dose ranges used no radiation effects on non-disjunction could be observed. The results are interpreted to show that in class B oocytes (1) sublethal damage is due to chromosome breaks and/or lesions leading to breaks and (2) X-ray-induced dominant lethality is the consequence of chromosome damage (true dominant lethals).     

Incompatibility between X chromosome factor and pericentric heterochromatic region causes lethality in hybrids between Drosophila melanogaster and its sibling species

The Dobzhansky-Muller model posits that postzygotic reproductive isolation results from the evolution of incompatible epistatic interactions between species: alleles that function in the genetic background of one species can cause sterility or lethality in the genetic background of another species. Progress in identifying and characterizing factors involved in postzygotic isolation in Drosophila has remained slow, mainly because Drosophila melanogaster, with all of its genetic tools, forms dead or sterile hybrids when crossed to its sister species, D. simulans, D. sechellia, and D. mauritiana. To circumvent this problem, we used chromosome deletions and duplications from D. melanogaster to map two hybrid incompatibility loci in F(1) hybrids with its sister species. We mapped a recessive factor to the pericentromeric heterochromatin of the X chromosome in D. simulans and D. mauritiana, which we call heterochromatin hybrid lethal (hhl), which causes lethality in F(1) hybrid females with D. melanogaster. As F(1) hybrid males hemizygous for a D. mauritiana (or D. simulans) X chromosome are viable, the lethality of deficiency hybrid females implies that a dominant incompatible partner locus exists on the D. melanogaster X. Using small segments of the D. melanogaster X chromosome duplicated onto the Y chromosome, we mapped a dominant factor that causes hybrid lethality to a small 24-gene region of the D. melanogaster X. We provide evidence suggesting that it interacts with hhl(mau). The location of hhl is consistent with the emerging theme that hybrid incompatibilities in Drosophila involve heterochromatic regions and factors that interact with the heterochromatin.     

A New Hybrid Rescue Allele in Drosophila melanogaster

Crosses of Drosophila melanogaster females to males of its sibling species Drosophila simulans, Drosophila mauritiana and Drosophila sechellia produce no sons and daughters that are viable only at low temperatures. We describe here a novel rescue allele Df(1)EP307-1-2 isolated on the basis of its suppression of high temperature hybrid female lethality. Df(1)EP307-1-2 also rescues hybrid males to the pharate adult stage, the same stage at which it is lethal to D. melanogaster pure species males. Molecular analysis indicates that Df(1)EP307-1-2 is associated with a deletion of about 61 kb in the 9D region of the X chromosome. The structure of Df(1)EP307-1-2 suggests that it was formed by a process similar to P-element induced male recombination.     

Intron length evolution in Drosophila

I present data on the evolution of intron lengths among 3 closely related Drosophila species, D. melanogaster, Drosophila simulans, and Drosophila yakuba. Using D. yakuba as an outgroup, I mapped insertion and deletion mutations in 148 introns (spanning approximately 30 kb) to the D. melanogaster and D. simulans lineages. Intron length evolution in the 2 sister species has been different: in D. melanogaster, X-linked introns have increased slightly in size, whereas autosomal ones have decreased slightly in size; in D. simulans, both X-linked and autosomal introns have decreased in size. To understand the possible evolutionary causes of these lineage- and chromosome-specific patterns of intron evolution, I studied insertion-deletion (indel) polymorphism and divergence in D. melanogaster. Small insertion mutations segregate at elevated frequencies and enjoy elevated probabilities of fixation, particularly on the X chromosome. In contrast, there is no detectable X chromosome effect on fixations in D. simulans. These findings suggest X chromosome-specific selection or biased gene conversion-gap repair favoring insertions in D. melanogaster but not in D. simulans. These chromosome- and lineage-specific patterns of indel substitution are not easily explained by existing general population genetic models of intron length evolution. Genomic data from D. melanogaster further suggest that the forces described here affect introns and intergenic regions similarly.     

Functional and comparative genomic analysis of the piebald deletion region of mouse chromosome 14

Several developmentally important genomic regions map within the piebald deletion complex on distal mouse chromosome 14. We have combined computational gene prediction and comparative sequence analysis to characterize an approximately 4.3-Mb segment of the piebald region to identify candidate genes for the phenotypes presented by homozygous deletion mice. As a result we have ordered 13 deletion breakpoints, integrated the sequence with markers from a bacterial artificial chromosome (BAC) physical map, and identified 16 known or predicted genes and >1500 conserved sequence elements (CSEs) across the region. The candidate genes identified include Phr1 (formerly Pam) and Spry2, which are mouse homologs of genes required for development in Drosophila melanogaster. Gene content, order, and position are highly conserved between mouse chromosome 14 and the orthologous region of human chromosome 13. Our studies combining computational gene prediction with genetic and comparative genomic analyses provide insight regarding the functional composition and organization of this defined chromosomal region.