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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

Phenotype classification.Images showing the three classes of defect: gaps, or lack of tissue; fusion, and polarity reversal. Right panels show higher magnification views of the bristle pattern to illustrate the polarity reversal phenotype. Refers to Figure 1E.DOI:http://dx.doi.org/10.7554/eLife.07389.005
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fig1s2: Phenotype classification.Images showing the three classes of defect: gaps, or lack of tissue; fusion, and polarity reversal. Right panels show higher magnification views of the bristle pattern to illustrate the polarity reversal phenotype. Refers to Figure 1E.DOI:http://dx.doi.org/10.7554/eLife.07389.005

Mentions: Mutants lacking miR-965 had only minor effects on survival during development. Mutant adults appeared to be morphologically normal with the exception of defects in abdominal segmentation (Figure 1E). Among the affected individuals, the predominant defect was a dorsal gap in one or more abdominal segments, in some cases leading to segment fusion (Figure 1—figure supplement 2). In addition, formation of ectopic bristles associated with a polarity defect was observed in ∼15% of affected individuals (Figure 1—figure supplement 3). Polarity reversal was always accompanied by a gap or segment fusion phenotype. These defects were rescued by restoring miRNA expression using the miR-965 RMCE rescue allele (Figure 1E).


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

Verma P, Cohen SM - Elife (2015)

Phenotype classification.Images showing the three classes of defect: gaps, or lack of tissue; fusion, and polarity reversal. Right panels show higher magnification views of the bristle pattern to illustrate the polarity reversal phenotype. Refers to Figure 1E.DOI:http://dx.doi.org/10.7554/eLife.07389.005
© Copyright Policy
Related In: Results  -  Collection

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

fig1s2: Phenotype classification.Images showing the three classes of defect: gaps, or lack of tissue; fusion, and polarity reversal. Right panels show higher magnification views of the bristle pattern to illustrate the polarity reversal phenotype. Refers to Figure 1E.DOI:http://dx.doi.org/10.7554/eLife.07389.005
Mentions: Mutants lacking miR-965 had only minor effects on survival during development. Mutant adults appeared to be morphologically normal with the exception of defects in abdominal segmentation (Figure 1E). Among the affected individuals, the predominant defect was a dorsal gap in one or more abdominal segments, in some cases leading to segment fusion (Figure 1—figure supplement 2). In addition, formation of ectopic bristles associated with a polarity defect was observed in ∼15% of affected individuals (Figure 1—figure supplement 3). Polarity reversal was always accompanied by a gap or segment fusion phenotype. These defects were rescued by restoring miRNA expression using the miR-965 RMCE rescue allele (Figure 1E).

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