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09:17
Generation of Maternal Mutants Using zpc:cas9 Knock-in Zebrafish
Published on: July 22, 2025
851
Wolbachia-induced Cytoplasmic Incompatibility drives epigenetic and maternally-influenced post-embryonic defects
Claire Perez1, Jillian Porter1, Brandt Warecki1
1Department of Molecular, Cell, Developmental Biology, University of California, Santa Cruz, Santa Cruz, CA, USA.
Biorxiv : the Preprint Server for Biology
|April 27, 2026
Summary
Cytoplasmic Incompatibility (CI) in Drosophila melanogaster causes developmental defects and lethality. These phenotypes, linked to Wolbachia
Area of Science:
- Developmental Biology
- Genetics
- Microbiology
Background:
- Cytoplasmic Incompatibility (CI) is a reproductive manipulation strategy employed by Wolbachia bacteria.
- In CI, Wolbachia-infected sperm exhibit defects in paternal chromosome condensation, replication, and segregation.
- Previous research indicated CI causes developmental defects and lethality in D. simulans.
Purpose of the Study:
- To investigate CI-induced mitotic defects, lethality, and locomotor impairments in Drosophila melanogaster.
- To explore the influence of genetic background on CI-induced phenotypes.
- To examine the role of epigenetic mechanisms in mediating CI effects.
Main Methods:
- Comparative analysis of embryos, larvae, and adults from CI and Rescue crosses in D. melanogaster.
- Assessment of mitotic errors during gastrulation and larval lethality.
- Evaluation of locomotor activity in affected individuals.
- Analysis of CI-induced lethality across 13 genetically distinct Drosophila Genetic Reference Panel (DGRP) lines.
- Measurement of H3K27me1 chromatin mark levels in CI-derived embryos.
Main Results:
- D. melanogaster embryos from CI crosses showed significant mitotic defects during gastrulation and increased larval lethality, which were absent in Rescue crosses.
- Significant variation in CI-induced lethality was observed among different DGRP lines.
- Locomotor defects were identified in 3rd instar larvae and adults from CI crosses, also rescued in progeny of Rescue crosses.
- Elevated levels of the H3K27me1 chromatin mark were detected in CI-derived embryos.
Conclusions:
- Wolbachia-induced CI in D. melanogaster leads to delayed developmental and locomotor defects, potentially mediated by epigenetic mechanisms.
- The maternal genetic background and epigenetic factors, such as H3K27me1, influence the strength of CI phenotypes.
- A comprehensive assessment of CI strength should include pre- and post-hatching lethality and locomotor function.
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