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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

miR-965 expression in histoblasts.Top: design of the control and miR-965 sensor transgenes. EGFP was under control of the tubulin promoter. For the miR-965 sensor, 1 copy of a perfect miR-965 target sequence was placed into the SV40 UTR. Images showing GFP expression from the control sensor (left) and miR-965 sensor (middle) transgenes at 21 hr APF. Histoblast nests consist of small diploid histoblast cells (hb) surrounded by large polyploid larval epidermal cells (LEC). Nuclei were labeled with histone-RFP (red). Downregulation of GFP was lost when the transgene was placed in the KO1/KO2 miR-965 mutant background (right). Anterior (A), posterior (P). Scale bar: 100 µm.DOI:http://dx.doi.org/10.7554/eLife.07389.007
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fig2: miR-965 expression in histoblasts.Top: design of the control and miR-965 sensor transgenes. EGFP was under control of the tubulin promoter. For the miR-965 sensor, 1 copy of a perfect miR-965 target sequence was placed into the SV40 UTR. Images showing GFP expression from the control sensor (left) and miR-965 sensor (middle) transgenes at 21 hr APF. Histoblast nests consist of small diploid histoblast cells (hb) surrounded by large polyploid larval epidermal cells (LEC). Nuclei were labeled with histone-RFP (red). Downregulation of GFP was lost when the transgene was placed in the KO1/KO2 miR-965 mutant background (right). Anterior (A), posterior (P). Scale bar: 100 µm.DOI:http://dx.doi.org/10.7554/eLife.07389.007

Mentions: The abdominal segmentation defects observed in miR-965 mutants suggested that the miRNA might be required in the histoblasts. To visualize miR-965 activity, we made use of a sensor transgene consisting of a ubiquitously expressed GFP reporter with a perfect target site for miR-965 in the 3′ UTR. Sensors of this design allow miRNA activity to be visualized by downregulation of GFP (Brennecke et al., 2003). The control sensor, lacking the miRNA-target site, was expressed at comparable levels in the large polyploid LEC and in the smaller histoblast cells (hb, Figure 2). miR-965 sensor GFP levels were lower in the histoblast nests, compared to the adjacent larval cells, particularly in the histoblast cells near the edge of the nests (Figure 2). This difference was lost when the sensor was introduced into the miR-965 mutant background, providing evidence that the reduced GFP level in the histoblasts is due to miR-965-mediated repression (Figure 2).10.7554/eLife.07389.007Figure 2.miR-965 expression in histoblasts.


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

Verma P, Cohen SM - Elife (2015)

miR-965 expression in histoblasts.Top: design of the control and miR-965 sensor transgenes. EGFP was under control of the tubulin promoter. For the miR-965 sensor, 1 copy of a perfect miR-965 target sequence was placed into the SV40 UTR. Images showing GFP expression from the control sensor (left) and miR-965 sensor (middle) transgenes at 21 hr APF. Histoblast nests consist of small diploid histoblast cells (hb) surrounded by large polyploid larval epidermal cells (LEC). Nuclei were labeled with histone-RFP (red). Downregulation of GFP was lost when the transgene was placed in the KO1/KO2 miR-965 mutant background (right). Anterior (A), posterior (P). Scale bar: 100 µm.DOI:http://dx.doi.org/10.7554/eLife.07389.007
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4538364&req=5

fig2: miR-965 expression in histoblasts.Top: design of the control and miR-965 sensor transgenes. EGFP was under control of the tubulin promoter. For the miR-965 sensor, 1 copy of a perfect miR-965 target sequence was placed into the SV40 UTR. Images showing GFP expression from the control sensor (left) and miR-965 sensor (middle) transgenes at 21 hr APF. Histoblast nests consist of small diploid histoblast cells (hb) surrounded by large polyploid larval epidermal cells (LEC). Nuclei were labeled with histone-RFP (red). Downregulation of GFP was lost when the transgene was placed in the KO1/KO2 miR-965 mutant background (right). Anterior (A), posterior (P). Scale bar: 100 µm.DOI:http://dx.doi.org/10.7554/eLife.07389.007
Mentions: The abdominal segmentation defects observed in miR-965 mutants suggested that the miRNA might be required in the histoblasts. To visualize miR-965 activity, we made use of a sensor transgene consisting of a ubiquitously expressed GFP reporter with a perfect target site for miR-965 in the 3′ UTR. Sensors of this design allow miRNA activity to be visualized by downregulation of GFP (Brennecke et al., 2003). The control sensor, lacking the miRNA-target site, was expressed at comparable levels in the large polyploid LEC and in the smaller histoblast cells (hb, Figure 2). miR-965 sensor GFP levels were lower in the histoblast nests, compared to the adjacent larval cells, particularly in the histoblast cells near the edge of the nests (Figure 2). This difference was lost when the sensor was introduced into the miR-965 mutant background, providing evidence that the reduced GFP level in the histoblasts is due to miR-965-mediated repression (Figure 2).10.7554/eLife.07389.007Figure 2.miR-965 expression in histoblasts.

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