RNA silencing functions as an adaptive antiviral defense in both plants and animals. In turn, viruses commonly encode suppressors of RNA silencing, which enable them to mount productive infection. These inhibitor proteins may be exploited as reagents with which to probe mechanisms and functions of RNA silencing pathways. In this report, we describe transgenic Drosophila strains that allow inducible expression of the viral RNA silencing inhibitors Flock House virus-B2, Nodamura virus-B2, vaccinia virus-E3L, influenza A virus-NS1 and tombusvirus P19. Some of these, especially the B2 proteins, are effective transgenic inhibitors of double strand RNA-induced gene silencing in flies. On the other hand, none of them is effective against the Drosophila microRNA pathway. Their functional selectivity makes these viral silencing proteins useful reagents with which to study biological functions of the Drosophila RNA interference pathway.
Insulin-like growth factor 1 (Igf1) is important for skin development and homoeostasis. However, overexpression and inactivation studies have produced variable findings regarding its role in hair follicle (HF) biology. Here, we studied a conditional and inducible knockout of the Igf1 receptor (Igf1r) in keratin 15-expressing bulge cells. Deletion of Igf1r after the development of the skin appendages in K15-Igf1r mice showed no abnormalities in epidermal homoeostasis. Numbers of bulge cells were lower in K15-Igf1r mice than in controls, without consequences on wound healing, at least in young mice. K15-Igf1r HFs entered anagen phase earlier than controls and showed a delay in the anagen/catagen switch. The expression of Bmp-4 mRNA was inhibited in HFs from K15-Igf1r . MED1 transcription was impaired in the epidermis of K15-Igf1r mice. These findings suggest that Igf1r controls the hair cycle, partly through Bmp-4 activation.
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