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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

(A) Predicted miR-965 sites in the string 3′UTR.Based on the potential for strong 3′ pairing in the Seed 1 mutant (shown in Figure 4D), as well as the presence of a second nearby non-canonical seed match (seed 2), a more extensively mutated UTR was made to eliminate pairing to both potential sites. Nucleotides mutated are shown in red. Refers to Figure 4D. (B) Structure of the miR-965 site in the string 3′ UTR, as predicted by RNAHybrid (http://bibiserv.techfak.uni---bielefeld.de/).DOI:http://dx.doi.org/10.7554/eLife.07389.020
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fig4s1: (A) Predicted miR-965 sites in the string 3′UTR.Based on the potential for strong 3′ pairing in the Seed 1 mutant (shown in Figure 4D), as well as the presence of a second nearby non-canonical seed match (seed 2), a more extensively mutated UTR was made to eliminate pairing to both potential sites. Nucleotides mutated are shown in red. Refers to Figure 4D. (B) Structure of the miR-965 site in the string 3′ UTR, as predicted by RNAHybrid (http://bibiserv.techfak.uni---bielefeld.de/).DOI:http://dx.doi.org/10.7554/eLife.07389.020

Mentions: The wg 3′UTR was used to make a luciferase reporter transgene and tested for regulation by miR-965 in S2 cells. miR-965 expression reduced wg 3′UTR reporter activity, and this regulation was lost in the wg UTR reporter mutated to disrupt pairing with the miRNA seed sequence (Figure 4C, mutated residues shown in red). miR-965 expression also reduced expression of the string 3′UTR luciferase reporter (Figure 4D). Mutation of the predicted target site to disrupt seed pairing partially offset regulation of the string 3′UTR luciferase reporter (Figure 4D, mutated residues in red). We noted the presence of a second potential target site nearby (Figure 4—figure supplement 1). More extensive mutation to disrupt both sites further compromised regulation by miR-965 (Figure 4D). Other non-canonical target sites might be responsible for the remaining regulation by miR-965, however, we do not exclude the possibility that there could also be indirect effects of miR-965 on expression of this reporter. These findings provide evidence that miR-965 can regulate expression of string and wg.


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

Verma P, Cohen SM - Elife (2015)

(A) Predicted miR-965 sites in the string 3′UTR.Based on the potential for strong 3′ pairing in the Seed 1 mutant (shown in Figure 4D), as well as the presence of a second nearby non-canonical seed match (seed 2), a more extensively mutated UTR was made to eliminate pairing to both potential sites. Nucleotides mutated are shown in red. Refers to Figure 4D. (B) Structure of the miR-965 site in the string 3′ UTR, as predicted by RNAHybrid (http://bibiserv.techfak.uni---bielefeld.de/).DOI:http://dx.doi.org/10.7554/eLife.07389.020
© Copyright Policy
Related In: Results  -  Collection

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

fig4s1: (A) Predicted miR-965 sites in the string 3′UTR.Based on the potential for strong 3′ pairing in the Seed 1 mutant (shown in Figure 4D), as well as the presence of a second nearby non-canonical seed match (seed 2), a more extensively mutated UTR was made to eliminate pairing to both potential sites. Nucleotides mutated are shown in red. Refers to Figure 4D. (B) Structure of the miR-965 site in the string 3′ UTR, as predicted by RNAHybrid (http://bibiserv.techfak.uni---bielefeld.de/).DOI:http://dx.doi.org/10.7554/eLife.07389.020
Mentions: The wg 3′UTR was used to make a luciferase reporter transgene and tested for regulation by miR-965 in S2 cells. miR-965 expression reduced wg 3′UTR reporter activity, and this regulation was lost in the wg UTR reporter mutated to disrupt pairing with the miRNA seed sequence (Figure 4C, mutated residues shown in red). miR-965 expression also reduced expression of the string 3′UTR luciferase reporter (Figure 4D). Mutation of the predicted target site to disrupt seed pairing partially offset regulation of the string 3′UTR luciferase reporter (Figure 4D, mutated residues in red). We noted the presence of a second potential target site nearby (Figure 4—figure supplement 1). More extensive mutation to disrupt both sites further compromised regulation by miR-965 (Figure 4D). Other non-canonical target sites might be responsible for the remaining regulation by miR-965, however, we do not exclude the possibility that there could also be indirect effects of miR-965 on expression of this reporter. These findings provide evidence that miR-965 can regulate expression of string and wg.

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