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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

EcR 3′ UTR reporter expression in the miR-965 mutant.A reporter transgene containing the n EcR 3′ UTR linked to GFP was introduced into the miR-965 KO1/KO2 mutant background. GFP expression (green) did not increase in the histoblast nests in the miRNA mutant compared to the control. Thus, there was no indication that the miRNA acts directly on EcR transcript. There were no good quality miR-965 sites predicted in the various EcR 3′ UTR isoforms. Nuclei were labeled with H2-RFP. Scale bar—100 µM. Refers to Figure 6D.DOI:http://dx.doi.org/10.7554/eLife.07389.033
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fig6s2: EcR 3′ UTR reporter expression in the miR-965 mutant.A reporter transgene containing the n EcR 3′ UTR linked to GFP was introduced into the miR-965 KO1/KO2 mutant background. GFP expression (green) did not increase in the histoblast nests in the miRNA mutant compared to the control. Thus, there was no indication that the miRNA acts directly on EcR transcript. There were no good quality miR-965 sites predicted in the various EcR 3′ UTR isoforms. Nuclei were labeled with H2-RFP. Scale bar—100 µM. Refers to Figure 6D.DOI:http://dx.doi.org/10.7554/eLife.07389.033

Mentions: In the course of this analysis, we observed that EcR transcript levels increased in the miR-965 mutant (Figure 6D). Both mature and primary transcript levels increased, suggesting an indirect effect of the miRNA on EcR transcription. To ask if there might also be a post-transcriptional component to the regulation of EcR by miR-965, we used an EcR 3′ UTR reporter transgene linked to GFP (Varghese and Cohen, 2007). GFP expression in the histoblast nests did not increase in the miRNA mutant background, indicating indirect regulation of EcR by miR-965 (Figure 6—figure supplement 2). These experiments provide evidence for a regulatory feedback relationship between miR-965 and the Ecdysone receptor (Figure 6E). EcR activity limits miR-965 expression. miR-965 activity limits EcR primary transcript levels, suggesting an effect on transcription.


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

Verma P, Cohen SM - Elife (2015)

EcR 3′ UTR reporter expression in the miR-965 mutant.A reporter transgene containing the n EcR 3′ UTR linked to GFP was introduced into the miR-965 KO1/KO2 mutant background. GFP expression (green) did not increase in the histoblast nests in the miRNA mutant compared to the control. Thus, there was no indication that the miRNA acts directly on EcR transcript. There were no good quality miR-965 sites predicted in the various EcR 3′ UTR isoforms. Nuclei were labeled with H2-RFP. Scale bar—100 µM. Refers to Figure 6D.DOI:http://dx.doi.org/10.7554/eLife.07389.033
© Copyright Policy
Related In: Results  -  Collection

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

fig6s2: EcR 3′ UTR reporter expression in the miR-965 mutant.A reporter transgene containing the n EcR 3′ UTR linked to GFP was introduced into the miR-965 KO1/KO2 mutant background. GFP expression (green) did not increase in the histoblast nests in the miRNA mutant compared to the control. Thus, there was no indication that the miRNA acts directly on EcR transcript. There were no good quality miR-965 sites predicted in the various EcR 3′ UTR isoforms. Nuclei were labeled with H2-RFP. Scale bar—100 µM. Refers to Figure 6D.DOI:http://dx.doi.org/10.7554/eLife.07389.033
Mentions: In the course of this analysis, we observed that EcR transcript levels increased in the miR-965 mutant (Figure 6D). Both mature and primary transcript levels increased, suggesting an indirect effect of the miRNA on EcR transcription. To ask if there might also be a post-transcriptional component to the regulation of EcR by miR-965, we used an EcR 3′ UTR reporter transgene linked to GFP (Varghese and Cohen, 2007). GFP expression in the histoblast nests did not increase in the miRNA mutant background, indicating indirect regulation of EcR by miR-965 (Figure 6—figure supplement 2). These experiments provide evidence for a regulatory feedback relationship between miR-965 and the Ecdysone receptor (Figure 6E). EcR activity limits miR-965 expression. miR-965 activity limits EcR primary transcript levels, suggesting an effect on transcription.

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