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miR-965 controls cell proliferation and migration during tissue morphogenesis in the Drosophila abdomen.

Verma P, Cohen SM - Elife (2015)

Bottom Line: During pupal development, the abdominal histoblast cells proliferate and migrate to replace the larval epidermis.Ecdysone signaling downregulates miR-965 at the onset of pupariation, linking activation of the histoblast nests to the hormonal control of metamorphosis.By regulating both cell proliferation and cell migration, miR-965 contributes to the robustness of this morphogenetic system.

View Article: PubMed Central - PubMed

Affiliation: Institute of Molecular and Cell Biology, Singapore, Singapore.

ABSTRACT
Formation of the Drosophila adult abdomen involves a process of tissue replacement in which larval epidermal cells are replaced by adult cells. The progenitors of the adult epidermis are specified during embryogenesis and, unlike the imaginal discs that make up the thoracic and head segments, they remain quiescent during larval development. During pupal development, the abdominal histoblast cells proliferate and migrate to replace the larval epidermis. Here, we provide evidence that the microRNA, miR-965, acts via string and wingless to control histoblast proliferation and migration. Ecdysone signaling downregulates miR-965 at the onset of pupariation, linking activation of the histoblast nests to the hormonal control of metamorphosis. Replacement of the larval epidermis by adult epidermal progenitors involves regulation of both cell-intrinsic events and cell communication. By regulating both cell proliferation and cell migration, miR-965 contributes to the robustness of this morphogenetic system.

No MeSH data available.


Related in: MedlinePlus

Large polyploid cells in miR-965 mutant histoblast nests.Histoblast nests were labeled with esg-Gal4-directed expression of UAS-GFP at 24 hr APF. Note the presence of large polyploid cells in the histoblast nest in the miR-965 mutant (arrows). At the start of the imaging period, the large polyploid cells marked by the arrows did not express GFP, but began to express GFP after making contact with the expanding histoblast nests. Possible explanations for the appearance of GFP in large polyploidy cells include (1) induction of esg-Gal4 activity in the larval cells that cannot be eliminated by the expanding histoblast nests, perhaps by signals from the histoblasts; (2) fusion of polyploidy LEC with esg-Gal4-expressing histoblasts. Scale bar: 50 µm. Refers to Figure 3B.DOI:http://dx.doi.org/10.7554/eLife.07389.010
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fig3s2: Large polyploid cells in miR-965 mutant histoblast nests.Histoblast nests were labeled with esg-Gal4-directed expression of UAS-GFP at 24 hr APF. Note the presence of large polyploid cells in the histoblast nest in the miR-965 mutant (arrows). At the start of the imaging period, the large polyploid cells marked by the arrows did not express GFP, but began to express GFP after making contact with the expanding histoblast nests. Possible explanations for the appearance of GFP in large polyploidy cells include (1) induction of esg-Gal4 activity in the larval cells that cannot be eliminated by the expanding histoblast nests, perhaps by signals from the histoblasts; (2) fusion of polyploidy LEC with esg-Gal4-expressing histoblasts. Scale bar: 50 µm. Refers to Figure 3B.DOI:http://dx.doi.org/10.7554/eLife.07389.010

Mentions: LEC generally undergo programmed cell death as the histoblasts nests start to grow (Nakajima et al., 2011). In miR-965 mutants, we observed that some of these cells were still present in the nests, suggesting a failure to eliminate LECs in the mutant (Figure 3—figure supplement 2). Delayed expansion of the histoblast nests, combined with the persistence of LECs, is likely to be responsible for the gaps observed in adult abdominal segments.


miR-965 controls cell proliferation and migration during tissue morphogenesis in the Drosophila abdomen.

Verma P, Cohen SM - Elife (2015)

Large polyploid cells in miR-965 mutant histoblast nests.Histoblast nests were labeled with esg-Gal4-directed expression of UAS-GFP at 24 hr APF. Note the presence of large polyploid cells in the histoblast nest in the miR-965 mutant (arrows). At the start of the imaging period, the large polyploid cells marked by the arrows did not express GFP, but began to express GFP after making contact with the expanding histoblast nests. Possible explanations for the appearance of GFP in large polyploidy cells include (1) induction of esg-Gal4 activity in the larval cells that cannot be eliminated by the expanding histoblast nests, perhaps by signals from the histoblasts; (2) fusion of polyploidy LEC with esg-Gal4-expressing histoblasts. Scale bar: 50 µm. Refers to Figure 3B.DOI:http://dx.doi.org/10.7554/eLife.07389.010
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4538364&req=5

fig3s2: Large polyploid cells in miR-965 mutant histoblast nests.Histoblast nests were labeled with esg-Gal4-directed expression of UAS-GFP at 24 hr APF. Note the presence of large polyploid cells in the histoblast nest in the miR-965 mutant (arrows). At the start of the imaging period, the large polyploid cells marked by the arrows did not express GFP, but began to express GFP after making contact with the expanding histoblast nests. Possible explanations for the appearance of GFP in large polyploidy cells include (1) induction of esg-Gal4 activity in the larval cells that cannot be eliminated by the expanding histoblast nests, perhaps by signals from the histoblasts; (2) fusion of polyploidy LEC with esg-Gal4-expressing histoblasts. Scale bar: 50 µm. Refers to Figure 3B.DOI:http://dx.doi.org/10.7554/eLife.07389.010
Mentions: LEC generally undergo programmed cell death as the histoblasts nests start to grow (Nakajima et al., 2011). In miR-965 mutants, we observed that some of these cells were still present in the nests, suggesting a failure to eliminate LECs in the mutant (Figure 3—figure supplement 2). Delayed expansion of the histoblast nests, combined with the persistence of LECs, is likely to be responsible for the gaps observed in adult abdominal segments.

Bottom Line: During pupal development, the abdominal histoblast cells proliferate and migrate to replace the larval epidermis.Ecdysone signaling downregulates miR-965 at the onset of pupariation, linking activation of the histoblast nests to the hormonal control of metamorphosis.By regulating both cell proliferation and cell migration, miR-965 contributes to the robustness of this morphogenetic system.

View Article: PubMed Central - PubMed

Affiliation: Institute of Molecular and Cell Biology, Singapore, Singapore.

ABSTRACT
Formation of the Drosophila adult abdomen involves a process of tissue replacement in which larval epidermal cells are replaced by adult cells. The progenitors of the adult epidermis are specified during embryogenesis and, unlike the imaginal discs that make up the thoracic and head segments, they remain quiescent during larval development. During pupal development, the abdominal histoblast cells proliferate and migrate to replace the larval epidermis. Here, we provide evidence that the microRNA, miR-965, acts via string and wingless to control histoblast proliferation and migration. Ecdysone signaling downregulates miR-965 at the onset of pupariation, linking activation of the histoblast nests to the hormonal control of metamorphosis. Replacement of the larval epidermis by adult epidermal progenitors involves regulation of both cell-intrinsic events and cell communication. By regulating both cell proliferation and cell migration, miR-965 contributes to the robustness of this morphogenetic system.

No MeSH data available.


Related in: MedlinePlus