Summary
Bacteria live in environments where resources for growth are scarce and shared with other bacteria. The ability to inhibit the growth of other bacteria is thus favourable and most bacteria use multiple systems for such antagonistic interactions, including delivery of protein toxins to other bacteria (e.g. bacteriocins, type 6 secretion and contact-dependent growth inhibition systems). In addition to their role in competition, all these toxin delivery systems frequently deliver toxins to cells of the same genotype, i.e. cells immune to the toxic activity, but a function for self-delivery of toxins has never been identified. Recent evidence from our lab suggests that self-delivery of toxins generates population heterogeneity in terms of growth at high cell densities, i.e. upon cell-cell contacts. But if this is a common feature of all toxin delivery systems is not known. Here we will investigate if toxin delivery to cells immune to the toxin creates population heterogeneity in terms of growth, mutation rates and gene expression, and if this is important for bacterial evolution and multicellularity. As homologs for many of the toxins can also be found in eukaryotes, including multicellular organisms, we will investigate if the functions of these systems are also conserved across kingdoms.
We will particular characterize the role of bacterial toxin delivery systems for multicellular behaviour and adaptation to new growth environments. This research have important consequences for understanding cell-to-cell contacts and the organization of multicellular tissues in general; from how to control biofilm formation to the understanding of uncontrolled cell growth in higher eukaryotes.
We will particular characterize the role of bacterial toxin delivery systems for multicellular behaviour and adaptation to new growth environments. This research have important consequences for understanding cell-to-cell contacts and the organization of multicellular tissues in general; from how to control biofilm formation to the understanding of uncontrolled cell growth in higher eukaryotes.
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More information & hyperlinks
| Web resources: | https://cordis.europa.eu/project/id/804068 |
| Start date: | 01-01-2019 |
| End date: | 31-12-2023 |
| Total budget - Public funding: | 1 499 765,00 Euro - 1 499 765,00 Euro |
Cordis data
Original description
Bacteria live in environments where resources for growth are scarce and shared with other bacteria. The ability to inhibit the growth of other bacteria is thus favourable and most bacteria use multiple systems for such antagonistic interactions, including delivery of protein toxins to other bacteria (e.g. bacteriocins, type 6 secretion and contact-dependent growth inhibition systems). In addition to their role in competition, all these toxin delivery systems frequently deliver toxins to cells of the same genotype, i.e. cells immune to the toxic activity, but a function for self-delivery of toxins has never been identified. Recent evidence from our lab suggests that self-delivery of toxins generates population heterogeneity in terms of growth at high cell densities, i.e. upon cell-cell contacts. But if this is a common feature of all toxin delivery systems is not known. Here we will investigate if toxin delivery to cells immune to the toxin creates population heterogeneity in terms of growth, mutation rates and gene expression, and if this is important for bacterial evolution and multicellularity. As homologs for many of the toxins can also be found in eukaryotes, including multicellular organisms, we will investigate if the functions of these systems are also conserved across kingdoms.We will particular characterize the role of bacterial toxin delivery systems for multicellular behaviour and adaptation to new growth environments. This research have important consequences for understanding cell-to-cell contacts and the organization of multicellular tissues in general; from how to control biofilm formation to the understanding of uncontrolled cell growth in higher eukaryotes.
Status
SIGNEDCall topic
ERC-2018-STGUpdate Date
27-04-2024
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