Acta Entomologica Sinica ›› 2023, Vol. 66 ›› Issue (7): 959-968.doi: 10.16380/j.kcxb.2023.07.010

• REVIEW ARTICLES • Previous Articles     Next Articles

Hybrid dysgenesis and P-element transposition in Drosophila

WANG Chun-Ming   

  1.  (School of Life Sciences, Lanzhou University, Lanzhou 730000, China)
  • Online:2023-07-20 Published:2023-08-17

Abstract: 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 are also arranged in cluster, called piRNA cluster. The piRNA cluster transcribes a single-stranded RNA precursor molecule, splices to 23-32 nt piRNA, then binds to the PIWI protein to form a complex, and plays a role through two pathways: One is to degrade the target mRNA complementary to the piRNA sequence and play a post-transcriptional silencing effect; the other is to enter the nucleus, guide the epigenetic modification of the sequence of P-element or piRNA cluster, play a transcriptional inhibition of P-element, and play a transcriptional activation effect on piRNA cluster. It was found that both the repressor mechanism and the piRNA mechanism play a role in the regulation of P-element transposition. This review may help with the teaching and scientific research of the phenomenon of hybrid dysgenesis.

Key words: Drosophila, hybrid dysgenesis, transposable elements, transposon, P-element, piRNA, repressor