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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

Still images from a time-lapse video of esg-Gal4>UAS-string histoblasts.Left: rapid proliferation phase. Note the presence of cells of different sizes, indicative of asynchronous division. Images represent 0 hr and mitosis M1, M2 and M3. Genotype: esg-Gal4, UAS-string, UAS-GFP. Right: growth and migration phase. Note the delayed spreading and incomplete replacement of the LEC, compared to controls at the equivalent time points (Figure 3C). Genotype: esg-Gal4, UAS-string, UAS-GFP. Refers to Figure 5B and Videos 8, 9.DOI:http://dx.doi.org/10.7554/eLife.07389.023
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fig5s2: Still images from a time-lapse video of esg-Gal4>UAS-string histoblasts.Left: rapid proliferation phase. Note the presence of cells of different sizes, indicative of asynchronous division. Images represent 0 hr and mitosis M1, M2 and M3. Genotype: esg-Gal4, UAS-string, UAS-GFP. Right: growth and migration phase. Note the delayed spreading and incomplete replacement of the LEC, compared to controls at the equivalent time points (Figure 3C). Genotype: esg-Gal4, UAS-string, UAS-GFP. Refers to Figure 5B and Videos 8, 9.DOI:http://dx.doi.org/10.7554/eLife.07389.023

Mentions: To ask whether the increases in string and wg expression might be responsible for the miR-965 mutant phenotype, we first asked if overexpressing them in an otherwise normal genetic background could phenocopy the mutant. esg-Gal4 driven expression of a UAS-string transgene produced abdominal segment gaps, segment fusion and polarity reversal phenotypes, similar to those observed in the miR-965 mutant (Figure 5AFigure 5—figure supplement 1). The proportion of flies with defects caused by string overexpression was similar to that in the miR-965 mutant (Figure 5B). string overexpression caused asynchronous histoblast division and apoptosis during the early division phase (Figure 5—figure supplement 2, Video 8). Expansion of the string-overexpressing histoblast nests was slowed, and the histoblasts were unable to fully replace the LECs (Figure 5—figure supplements 2, 3, Video 9), similar to what was observed in miR-965 mutants. Thus, string overexpression was sufficient to reproduce the miR-965 mutant phenotype.10.7554/eLife.07389.021Figure 5.Overexpression of string and wg contributes to the miR-965 mutant phenotype.


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

Verma P, Cohen SM - Elife (2015)

Still images from a time-lapse video of esg-Gal4>UAS-string histoblasts.Left: rapid proliferation phase. Note the presence of cells of different sizes, indicative of asynchronous division. Images represent 0 hr and mitosis M1, M2 and M3. Genotype: esg-Gal4, UAS-string, UAS-GFP. Right: growth and migration phase. Note the delayed spreading and incomplete replacement of the LEC, compared to controls at the equivalent time points (Figure 3C). Genotype: esg-Gal4, UAS-string, UAS-GFP. Refers to Figure 5B and Videos 8, 9.DOI:http://dx.doi.org/10.7554/eLife.07389.023
© Copyright Policy
Related In: Results  -  Collection

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

fig5s2: Still images from a time-lapse video of esg-Gal4>UAS-string histoblasts.Left: rapid proliferation phase. Note the presence of cells of different sizes, indicative of asynchronous division. Images represent 0 hr and mitosis M1, M2 and M3. Genotype: esg-Gal4, UAS-string, UAS-GFP. Right: growth and migration phase. Note the delayed spreading and incomplete replacement of the LEC, compared to controls at the equivalent time points (Figure 3C). Genotype: esg-Gal4, UAS-string, UAS-GFP. Refers to Figure 5B and Videos 8, 9.DOI:http://dx.doi.org/10.7554/eLife.07389.023
Mentions: To ask whether the increases in string and wg expression might be responsible for the miR-965 mutant phenotype, we first asked if overexpressing them in an otherwise normal genetic background could phenocopy the mutant. esg-Gal4 driven expression of a UAS-string transgene produced abdominal segment gaps, segment fusion and polarity reversal phenotypes, similar to those observed in the miR-965 mutant (Figure 5AFigure 5—figure supplement 1). The proportion of flies with defects caused by string overexpression was similar to that in the miR-965 mutant (Figure 5B). string overexpression caused asynchronous histoblast division and apoptosis during the early division phase (Figure 5—figure supplement 2, Video 8). Expansion of the string-overexpressing histoblast nests was slowed, and the histoblasts were unable to fully replace the LECs (Figure 5—figure supplements 2, 3, Video 9), similar to what was observed in miR-965 mutants. Thus, string overexpression was sufficient to reproduce the miR-965 mutant phenotype.10.7554/eLife.07389.021Figure 5.Overexpression of string and wg contributes to the miR-965 mutant phenotype.

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