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c-di-GMP induction of Dictyostelium cell death requires the polyketide DIF-1.

Song Y, Luciani MF, Giusti C, Golstein P - Mol. Biol. Cell (2014)

Bottom Line: In these cases, c-di-GMP-induced cell death was rescued by complementation with exogenous DIF-1.Taken together, these results demonstrated that c-di-GMP could trigger cell death in Dictyostelium only in the presence of the DIF-1 polyketide or its metabolites.This identified another element of control to this cell death and perhaps also to c-di-GMP effects in other situations and organisms.

View Article: PubMed Central - PubMed

Affiliation: Centre d'Immunologie de Marseille-Luminy, UM2 Aix-Marseille Université; Institut National de la Santé et de la Recherche Médicale, U1104; and Centre National de la Recherche Scientifique, UMR7280, 13288 Marseille, France.

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Mutation of the DmtA methylase prevented vacuolization by exogenous c-di-GMP. c-di-GMP–induced vacuolization was prevented by a DmtA mutation, which did not affect vacuolization induced by exogenous DIF-1 or by DIF-1 and c-di-GMP. Numbers are percentages of vacuolization as in the legend to Figure 1A. These results showed that DmtA-dependent polyketides, namely DIF-1 and/or its metabolites, were required for c-di-GMP–induced cell death. The differences in the extent of inhibition of vacuolization between DmtA− cells in this figure and StlB− cells in Figure 3 likely reflect the differences in the kinetics/extent of vacuolization of control DH1 parental cells between these experiments.
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Figure 4: Mutation of the DmtA methylase prevented vacuolization by exogenous c-di-GMP. c-di-GMP–induced vacuolization was prevented by a DmtA mutation, which did not affect vacuolization induced by exogenous DIF-1 or by DIF-1 and c-di-GMP. Numbers are percentages of vacuolization as in the legend to Figure 1A. These results showed that DmtA-dependent polyketides, namely DIF-1 and/or its metabolites, were required for c-di-GMP–induced cell death. The differences in the extent of inhibition of vacuolization between DmtA− cells in this figure and StlB− cells in Figure 3 likely reflect the differences in the kinetics/extent of vacuolization of control DH1 parental cells between these experiments.

Mentions: Which stlB-dependent polyketide(s) cooperate(s) with c-di-GMP? Within the stlB-dependent biosynthetic cascade (Supplemental Figure S4), the DmtA methyltransferase catalyzed the last step to DIF-1 biosynthesis. We disrupted the DmtA gene in DH1 cells (Supplemental Figure S6), previously disrupted in strain AX2 (Thompson and Kay, 2000). DH1.DmtA− cells, which vacuolized as well as DH1 cells upon addition of DIF-1 or of both DIF-1 and c-di-GMP (Figure 4), when subjected to c-di-GMP vacuolized much less than DH1 cells (Figure 4). Thus cell death induction by c-di-GMP required polyketides depending on the DmtA methylase, namely DIF-1 and/or its metabolites (Traynor and Kay, 1991).


c-di-GMP induction of Dictyostelium cell death requires the polyketide DIF-1.

Song Y, Luciani MF, Giusti C, Golstein P - Mol. Biol. Cell (2014)

Mutation of the DmtA methylase prevented vacuolization by exogenous c-di-GMP. c-di-GMP–induced vacuolization was prevented by a DmtA mutation, which did not affect vacuolization induced by exogenous DIF-1 or by DIF-1 and c-di-GMP. Numbers are percentages of vacuolization as in the legend to Figure 1A. These results showed that DmtA-dependent polyketides, namely DIF-1 and/or its metabolites, were required for c-di-GMP–induced cell death. The differences in the extent of inhibition of vacuolization between DmtA− cells in this figure and StlB− cells in Figure 3 likely reflect the differences in the kinetics/extent of vacuolization of control DH1 parental cells between these experiments.
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Related In: Results  -  Collection

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Figure 4: Mutation of the DmtA methylase prevented vacuolization by exogenous c-di-GMP. c-di-GMP–induced vacuolization was prevented by a DmtA mutation, which did not affect vacuolization induced by exogenous DIF-1 or by DIF-1 and c-di-GMP. Numbers are percentages of vacuolization as in the legend to Figure 1A. These results showed that DmtA-dependent polyketides, namely DIF-1 and/or its metabolites, were required for c-di-GMP–induced cell death. The differences in the extent of inhibition of vacuolization between DmtA− cells in this figure and StlB− cells in Figure 3 likely reflect the differences in the kinetics/extent of vacuolization of control DH1 parental cells between these experiments.
Mentions: Which stlB-dependent polyketide(s) cooperate(s) with c-di-GMP? Within the stlB-dependent biosynthetic cascade (Supplemental Figure S4), the DmtA methyltransferase catalyzed the last step to DIF-1 biosynthesis. We disrupted the DmtA gene in DH1 cells (Supplemental Figure S6), previously disrupted in strain AX2 (Thompson and Kay, 2000). DH1.DmtA− cells, which vacuolized as well as DH1 cells upon addition of DIF-1 or of both DIF-1 and c-di-GMP (Figure 4), when subjected to c-di-GMP vacuolized much less than DH1 cells (Figure 4). Thus cell death induction by c-di-GMP required polyketides depending on the DmtA methylase, namely DIF-1 and/or its metabolites (Traynor and Kay, 1991).

Bottom Line: In these cases, c-di-GMP-induced cell death was rescued by complementation with exogenous DIF-1.Taken together, these results demonstrated that c-di-GMP could trigger cell death in Dictyostelium only in the presence of the DIF-1 polyketide or its metabolites.This identified another element of control to this cell death and perhaps also to c-di-GMP effects in other situations and organisms.

View Article: PubMed Central - PubMed

Affiliation: Centre d'Immunologie de Marseille-Luminy, UM2 Aix-Marseille Université; Institut National de la Santé et de la Recherche Médicale, U1104; and Centre National de la Recherche Scientifique, UMR7280, 13288 Marseille, France.

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