The <i>Drosophila</i> maternal-effect gene <i>abnormal oocyte</i> ( <i>ao</i> ) does not repress histone gene expression

The abnormal oocyte (ao) gene of Drosophila melanogaster is a maternal-effect lethal gene previously identified as encoding a transcriptional regulator of core histones. However, background genetic mutations in existing ao mutant strains could compromise their utility in manipulating histone levels. To distinguish the true ao phenotype from background effects, we created two new ao reagents: a CRISPR/Cas9-mediated knockout of the ao allele for genetic and molecular analyses and an epitope-tagged ao allele for cytological experiments. Using these reagents, we confirm previous findings that loss of ao causes maternal-effect lethality, which can be rescued by either a decrease in the histone gene copy number or by Y chromosome heterochromatin. Our data indicate that ao genetically interacts with the heterochromatin, as previously suggested. However, contrary to a prior study, we detected neither Ao localization to histone genes nor ao repression of core histone transcript levels. Thus, the molecular basis for ao-associated maternal-effect lethality remains unknown.

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Publication Details

Journal
Genetics
Published
2026-02-05
DOI
https://doi.org/10.1093/genetics/iyag036
Citations
1
Primary Topic
Genomics and Chromatin Dynamics
Type
article
Field-Weighted Citation Impact
22.24
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article

The Drosophila maternal-effect gene abnormal oocyte ( ao ) does not repress histone gene expression

Eric Albanese, Casey A. Schmidt, Leila E. Rieder, Risa Takenaka et al.
1 citations
Genetics
Genomics and Chromatin Dynamics
22.24
article

The Drosophila maternal-effect gene abnormal oocyte ( ao ) does not repress histone gene expression

Eric Albanese, Casey A. Schmidt, Leila E. Rieder, Risa Takenaka, Sierra M. Simmerman, Janet Young, Mandalay A E Maddox, Harmit S Malik, Shilpi Verghese
article en
1 citations

Abstract

The abnormal oocyte (ao) gene of Drosophila melanogaster is a maternal-effect lethal gene previously identified as encoding a transcriptional regulator of core histones. However, background genetic mutations in existing ao mutant strains could compromise their utility in manipulating histone levels. To distinguish the true ao phenotype from background effects, we created two new ao reagents: a CRISPR/Cas9-mediated knockout of the ao allele for genetic and molecular analyses and an epitope-tagged ao allele for cytological experiments. Using these reagents, we confirm previous findings that loss of ao causes maternal-effect lethality, which can be rescued by either a decrease in the histone gene copy number or by Y chromosome heterochromatin. Our data indicate that ao genetically interacts with the heterochromatin, as previously suggested. However, contrary to a prior study, we detected neither Ao localization to histone genes nor ao repression of core histone transcript levels. Thus, the molecular basis for ao-associated maternal-effect lethality remains unknown.

Genetics
Cape Town HVTN Immunology Laboratory / Hutchinson Centre Research Institute of South Africa (ZA), Howard Hughes Medical Institute (US), Emory University (US), Lafayette College (US), University of Washington (US), Fred Hutch Cancer Center (US)
Openalex Percentile: Top 1%
Genomics and Chromatin Dynamics
22.24
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The <i>Drosophila</i> maternal-effect gene <i>abnormal oocyte</i> ( <i>ao</i> ) does not repress histone gene expression — Eric Albanese, Casey A. Schmidt, et al. · Genetics (2026) | TGRS Research Map | TGRS