Expression and localization of heat-shock proteins during skeletal muscle cell proliferation and differentiation and the impact of heat stress.

Skeletal myogenesis is a coordinated sequence of events associated with dramatic changes in cell morphology, motility, and metabolism, which causes cellular stress and alters proteostasis. Chaperones, such as heat-shock proteins (HSPs), play important roles in limiting cellular stresses and maintaining proteostasis, but whether HSPs are specifically involved in myogenesis is not well understood. Here, we characterized gene and protein expression and subcellular localization of various HSPs in proliferating C2C12 myoblasts and differentiating myotubes under control conditions and in response to heat stress.

The Ecdysone receptor constrains wingless expression to pattern cell cycle across the Drosophila wing margin in a Cyclin B-dependent manner.

Background: Ecdysone triggers transcriptional changes via the ecdysone receptor (EcR) to coordinate developmental programs of apoptosis, cell cycle and differentiation. Data suggests EcR affects cell cycle gene expression indirectly and here we identify Wingless as an intermediary factor linking EcR to cell cycle.

Results: We demonstrate EcR patterns cell cycle across the presumptive Drosophila wing margin by constraining wg transcription to modulate CycB expression, but not the previously identified Wg-targets dMyc or Stg.

Genetic systems to investigate regulation of oncogenes and tumour suppressor genes in Drosophila.

Animal growth requires coordination of cell growth and cell cycle progression with developmental signaling. Loss of cell cycle control is extremely detrimental, with reduced cycles leading to impaired organ growth and excessive proliferation, potentially resulting in tissue overgrowth and driving tumour initiation. Due to the high level of conservation between the cell cycle machinery of Drosophila and humans, the appeal of the fly model continues to be the means with which we can use sophisticated genetics to provide novel insights into mammalian growth and cell cycle control.

Hfp, the Drosophila homolog of the mammalian c-myc transcriptional-repressor and tumor suppressor FIR, inhibits dmyc transcription and cell growth.

Here we highlight our recent study, which revealed a mechanism critical for tight regulation of Drosophila myc (dmyc) transcription. Our previous work demonstrated that the RRM (RNA recognition motif) protein Half pint (Hfp) behaves as a growth and cell cycle inhibitor and work from D. Levens group has shown the mammalian ortholog, FIR (the FBP Interacting Repressor), is a tumor suppressor.

Hfp inhibits Drosophila myc transcription and cell growth in a TFIIH/Hay-dependent manner.

An unresolved question regarding the RNA-recognition motif (RRM) protein Half pint (Hfp) has been whether its tumour suppressor behaviour occurs by a transcriptional mechanism or via effects on splicing. The data presented here demonstrate that Hfp achieves cell cycle inhibition via an essential role in the repression of Drosophila myc (dmyc) transcription. We demonstrate that regulation of dmyc requires interaction between the transcriptional repressor Hfp and the DNA helicase subunit of TFIIH, Haywire (Hay).

Impact of steroid hormone signals on Drosophila cell cycle during development.

Metamorphosis of Drosophila involves proliferation, differentiation and death of larval tissues in order to form the adult fly. The major steroid hormone implicated in the larval-pupal transition and adult tissue modelling is ecdysone. Previous reviews have draw together studies connecting ecdysone signaling to the processes of apoptosis and differentiation.

The Ecdysone-inducible zinc-finger transcription factor Crol regulates Wg transcription and cell cycle progression in Drosophila.

The steroid hormone Ecdysone is crucial for developmental cell death, proliferation and morphogenesis in Drosophila. Herein, we delineate a molecular pathway linking Ecdysone signalling to cell cycle regulation in the Drosophila developing wing. We present evidence that the Ecdysone-inducible zinc-finger transcription factor Crol provides a crucial link between the Ecdysone steroid hormone pathway and the Wingless (Wg) signalling pathway in Drosophila.