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SDF-1 chemokine signaling modulates the apoptotic responses of clathrin-depleted DT40 cells

ABSTRACT: The cell line DKO-S is derived form chicken B-Cell DT40 cells where the clathrin heavy-chain has been placed under the control of a tetracycline-regulatable promoter (Tet-Off). The originally derived cell-line DKO-S underwent apoptosis when clathrin expression was repressed. A cell line, DKO-R, derived from DKO-S cells that was less sensitive to clathrin-depletion. This project explores the differnces in gene expression between DKO-R and DKO-S cells

ORGANISM(S): Gallus gallus

PROVIDER: GSE57328 | GEO | 2014/05/07

SECONDARY ACCESSION(S): PRJNA246282

REPOSITORIES: GEO

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SDF-1 chemokine signaling modulates the apoptotic responses of clathrin-depleted DT40 cells

Project description:The cell line DKO-S is derived form chicken B-Cell DT40 cells where the clathrin heavy-chain has been placed under the control of a tetracycline-regulatable promoter (Tet-Off). The originally derived cell-line DKO-S underwent apoptosis when clathrin expression was repressed. A cell line, DKO-R, derived from DKO-S cells that was less sensitive to clathrin-depletion. This project explores the differnces in gene expression between DKO-R and DKO-S cells Duplicate samples ofDT40, DKO-S or DKO_R cells either with or without treatment with deoxycyclin are compared as is the expression between DKO-R and DKO-S cell lines

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SDF-1 chemokine signalling modulates the apoptotic responses to iron deprivation of clathrin-depleted DT40 cells.

Project description:We have previously deleted both endogenous copies of the clathrin heavy-chain gene in the chicken pre B-cell-line DT40 and replaced them with clathrin under the control of a tetracycline-regulatable promoter (Tet-Off). The originally derived cell-line DKO-S underwent apoptosis when clathrin expression was repressed. We have also described a cell-line DKO-R derived from DKO-S cells that was less sensitive to clathrin-depletion. Here we show that the restriction of transferrin uptake, resulting in iron deprivation, is responsible for the lethal consequence of clathrin-depletion. We further show that the DKO-R cells have up-regulated an anti-apoptotic survival pathway based on the chemokine SDF-1 and its receptor CXCR4. Our work clarifies several puzzling features of clathrin-depleted DT40 cells and reveals an example of how SDF-1/CXCR4 signalling can abrogate pro-apoptotic pathways and increase cell survival. We propose that the phenomenon described here has implications for the therapeutic approach to a variety of cancers.

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