Loss of Nuclear Protein Dyro Causes Abnormalities in Nurse Cell Nuclei and Abort Oogenesis at Mid‐Oogenesis Checkpoint
The mid‐oogenesis checkpoint in Drosophila melanogaster functions to optimize nutrient usage by triggering abortion of oogenesis when females are starved or when developmental defects arise in the egg chamber. In the Dyro mutant, which encodes a nuclear factor, oogenesis is aborted during stages 8–9...
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Published in | Genes to cells : devoted to molecular & cellular mechanisms Vol. 30; no. 5; p. e70045 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
England
01.09.2025
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Subjects | |
Online Access | Get full text |
ISSN | 1356-9597 1365-2443 1365-2443 |
DOI | 10.1111/gtc.70045 |
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Summary: | The mid‐oogenesis checkpoint in Drosophila melanogaster functions to optimize nutrient usage by triggering abortion of oogenesis when females are starved or when developmental defects arise in the egg chamber. In the Dyro mutant, which encodes a nuclear factor, oogenesis is aborted during stages 8–9, corresponding to the mid‐oogenesis checkpoint. To investigate the relationship between Dyro and this checkpoint, we analyzed the phenotype of the Dyro mutant. Mosaic analysis showed that loss of Dyro in germline cells results in female sterility. Although inhibition of programmed cell death suppressed germline cell death during oogenesis, it failed to rescue the fertility of Dyro mutants, suggesting that oogenesis arrest in the Dyro mutant is not due to misregulation of the cell death signal. We then examined germline cell defects in the Dyro mutant and observed morphological abnormalities in the nucleoli and chromosomes of nurse cells. The chromosomes in Dyro mutant nurse cells were not fully dispersed, and the nucleoli were confined to small spaces between thickened chromosomes. These findings suggest that Dyro plays an important role in nurse cells and that loss of Dyro leads to defects in the chromosomes and nuclei of nurse cells, which leads to abortion of oogenesis. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1356-9597 1365-2443 1365-2443 |
DOI: | 10.1111/gtc.70045 |