Related Experiment Video
Updated: Jul 30, 2026
08:54
Bimolecular Fluorescence Complementation
Published on: April 15, 2011
28.1K
cifB-transcript levels largely explain cytoplasmic incompatibility variation across divergent Wolbachia
J Dylan Shropshire1, Emily Hamant1, William R Conner1
1Division of Biological Sciences, University of Montana, Missoula, MT 59812, USA.
PNAS Nexus
|August 15, 2022
Summary
Wolbachia bacteria cause cytoplasmic incompatibility (CI) in Drosophila, impacting host fitness. CI strength is primarily determined by cifB-transcript levels in testes, influenced by host and bacterial evolution.
Area of Science:
- Microbial genetics
- Evolutionary biology
- Insect-microbe interactions
Background:
- Maternally transmitted Wolbachia bacteria are common endosymbionts influencing host fitness.
- Cytoplasmic incompatibility (CI) is a key mechanism driving Wolbachia spread, caused by cifA and cifB genes.
- Significant variation exists in CI strength among Wolbachia strains, with underlying reasons unclear.
Purpose of the Study:
- Investigate the mechanistic basis of CI strength variation in Drosophila Wolbachia.
- Analyze CI strength in a phylogenetic context across millions of years of Wolbachia evolution.
- Identify genetic and host factors contributing to differences in CI efficacy.
Main Methods:
- Phylogenetic analysis of Wolbachia evolution in Drosophila over 20-50 million years.
- Sequence analysis of diverse Cif proteins and structural prediction using AlphaFold.
- Quantification of cifB-transcript levels in testes and correlation with CI strength.
- Assessment of host larval stage length as a covariate.
Main Results:
- CifB protein sequence similarity does not predict structural similarity.
- cifB-transcript levels in testes largely explain variation in CI strength.
- Closely related Wolbachia strains exhibit similar CI strengths and cifB-transcript levels.
- Host larval life stage duration positively correlates with CI strength.
Conclusions:
- Bacterial cifB-transcript levels are the primary determinant of Wolbachia-induced CI strength.
- Non-cif genomic regions and host factors modulate CI efficacy.
- Understanding CI mechanisms is crucial for predicting Wolbachia spread and enhancing biocontrol strategies.
Related Concept Videos
02:32Position-effect Variegation
In 1928, a German botanist Emil Heitz observed the moss nuclei with a DNA binding dye. He observed that while some chromatin regions decondense and spread out in the interphase nucleus, others do not. He termed them euchromatin and heterochromatin, respectively. He proposed that the heterochromatin regions reflect a functionally inactive state of the genome. It was later confirmed that heterochromatin is transcriptionally repressed, and euchromatin is transcriptionally active chromatin.
02:02Cis-regulatory Sequences
Cis-regulatory sequences are short fragments of non-coding DNA that are present on the same chromosomes as the genes that they regulate. These fragments serve as binding sites for transcriptional regulators, proteins that are responsible for controlling gene transcription and differential gene expression across cell types in eukaryotes. Cis-regulatory sequences can be close to the gene of interest or thousands of bases away in the DNA sequence; however, those sequences that are further away are...
02:32Exon Recombination
The evolution of new genes is critical for speciation. Exon recombination, also known as exon shuffling or domain shuffling, is an important means of new gene formation. It is observed across vertebrates, invertebrates, and in some plants such as potatoes and sunflowers. During exon recombination, exons from the same or different genes recombine and produce new exon-intron combinations, which might evolve into new genes.
Exon shuffling follows “splice frame rules.” Each exon has three reading...
Exon shuffling follows “splice frame rules.” Each exon has three reading...