果蝇杂种劣育与P因子转座调控  

Hybrid dysgenesis and P-element transposition in Drosophila

作　　者：王春明[1] WANG Chun-Ming(School of Life Sciences,Lanzhou University,Lanzhou 730000,China)

机构地区：[1]兰州大学生命科学学院,兰州730000

出　　处：《昆虫学报》2023年第7期959-968,共10页Acta Entomologica Sinica

基　　金：兰州大学教育教学改革研究项目。

摘　　要：果蝇Drosophila杂种劣育(hybrid dysgenesis)指某些品系果蝇间杂交,子代出现诸如卵巢发育不全、分离比异常、雄性个体减数分裂出现重组、高突变率、高频率染色体畸变甚至不育等异常现象。该现象可由多种转座因子(transposable element,TE)频繁转座引起,包括:P因子、I因子、hobo因子、Penelope因子、Paris因子和Helena因子等。其中P因子是首个确定DNA序列的真核生物转座子,也是研究得最为充分的动物TE之一,已被开发成基因工程工具,在果蝇转基因研究中发挥重要作用。基因组中携带P因子的果蝇为父系品系(paternal strain),即P品系,无P因子的果蝇为母系品系(maternal strain),即M品系。M雌×P雄杂交子代,在繁殖过程中出现杂种劣育现象,而P雌×M雄、M雌×M雄以及P雌×P雄交配组合的后代都是正常的。近20年来,P因子调控机制研究取得重大进展,在原有阻遏蛋白机制外,又发现了与PIWI蛋白相互作用的RNA[P-element-induced wimpy testis(PIWI)-interacting RNA,piRNA]机制。阻遏蛋白机制基于P因子转座酶4个外显子间的3个内含子转录后剪切方式:如果3个内含子均被剪切,则产生的mRNA包含4个外显子,翻译为87 kD的转座酶,促进P因子转座;如果仅前2个内含子被剪切,则产生的mRNA在第3个内含子区段所含终止密码子处提前终止翻译,产生66 kD的阻遏蛋白,阻止P因子转座。近年发现的piRNA机制是更为普遍的TE调控机制,该机制类似细菌中发现的CRISPR来源的RNA(CRISPR-derived RNA,crRNA)机制,编码piRNA的基因也成簇排列,称为piRNA基因簇。piRNA基因簇转录出单链RNA前体分子,剪切为23~32 nt的piRNA,随即与PIWI蛋白结合形成复合体,并通过两个途径发挥作用:一是降解与piRNA序列互补的靶mRNA,发挥转录后沉默作用;另一是进入细胞核,指导P因子或piRNA基因簇序列的表观遗传修饰,发挥对P因子的转录抑制作用,和对piRNA基因簇的转录激活作用。Hybrid dysgenesis in Drosophila refers to the occurrence of some abnormal phenomena in the progeny when crossing certain strains of Drosophila,such as ovarian hypoplasia,abnormal segregation ratio,recombination in male meiosis,high mutation rate,high frequency of chromosomal aberrations,even leading to infertility of the progeny etc.Hybrid dysgenesis in Drosophila is caused by frequent transposition of the transposable element(TE),including P-element,I-element,hobo-element,Penelope-element,Paris-element,Helena-element etc.P-element is the first eukaryotic transposon to have its DNA sequence determined,and it is also one of the most well-studied animal transposons.Developed as a genetic engineering tool,P-element has played an important role in Drosophila transgenic research.Drosophila carrying P-element in the genome is paternal strain(P strain),while that without P-element is maternal strain(M strain).In a cross of M female×P male,the progeny shows hybrid dysgenesis,while the progeny of the mating combinations of P female×M male,M female×M male and P female×P male is normal.In the past 20 years,significant progress has been made in the research on the regulation mechanism of P-element.In addition to the original repressor mechanism,a piRNA[P-element-induced wimpy testis(PIWI)-interacting RNA]mechanism has been discovered.The repressor mechanism is based on the post-transcriptional splicing of three introns among four exons of P-element transposase.If all the three introns are spliced,the resulted mRNA contains four exons,which are translated into a 87 kD transposase,promoting P-element transposition.If only the first two introns are spliced,the resulted mRNA terminates translation prematurely at the stop codon contained in the 3rd intron segment,producing a 66 kD repressor that prevents P-element transposition.The piRNA mechanism discovered in recent years is a more common TE regulatory mechanism.The mechanism is similar to the CRISPR-derived RNA(crRNA)mechanism found in bacteria,and the genes encoding piRNA

关 键 词：果蝇 杂种劣育 转座因子 转座子 P因子 PIRNA 阻遏蛋白 

分 类 号：Q963[生物学—昆虫学]