RESUMEN
Cooperation is central to many major transitions in evolution, including the emergence of eukaryotic cells, multicellularity and eusociality. Cooperation can be destroyed by the spread of cheater mutants that do not cooperate but gain the benefits of cooperation from others. However, cooperation can be preserved if cheaters are facultative, cheating others but cooperating among themselves. Several cheater mutants have been studied before, but no study has attempted a genome-scale investigation of the genetic opportunities for cheating. Here we describe such a screen in a social amoeba and show that cheating is multifaceted by revealing cheater mutations in well over 100 genes of diverse types. Many of these mutants cheat facultatively, producing more than their fair share of spores in chimaeras, but cooperating normally when clonal. These findings indicate that phenotypically stable cooperative systems may nevertheless harbour genetic conflicts. The opportunities for evolutionary moves and countermoves in such conflicts may select for the involvement of multiple pathways and numerous genes.
Asunto(s)
Conducta Cooperativa , Dictyostelium/genética , Dictyostelium/fisiología , Mutación/genética , Conducta Social , Amoeba/genética , Amoeba/fisiología , Animales , Agregación Celular , Quimera/genética , Quimera/fisiología , Dictyostelium/citología , Genes Protozoarios/genética , Genoma/genética , Genómica , Myxococcus xanthus/genética , Myxococcus xanthus/fisiología , Fenotipo , Esporas Protozoarias/genética , Esporas Protozoarias/fisiologíaRESUMEN
Cell adhesion molecules play an important physical role in shaping the structure of multicellular organisms. Recent studies show that they also play a role in intracellular and intercellular signaling. We describe a cell adhesion pathway that is mediated by the intercellular communication genes comC, lagC, and lagD during Dictyostelium development. Disruptions of these genes result in strains that are unable to generate spores when developed in a pure population but are capable of sporulation when developed in chimerae with wild-type cells. In contrast, any pair-wise chimera of the three mutants fails to form spores. We postulate that the wild-type cells supply the mutant cells with a signal that partially rescues their sporulation. We also propose that the three mutants are deficient in the production of that signal, suggesting that the three genes function in one signaling pathway. In support of that notion, the mutant cells share common non-cell-autonomous prespore and prestalk-specific defects and a common pattern of developmental progression and regression. We provide transcriptional and functional evidence for a network in which comC inhibits lagC and activates lagD expression, lagC and lagD are mutually inductive, and the cell adhesion gene lagC is the terminal node in this signaling network.
Asunto(s)
Adhesión Celular , Comunicación Celular , Dictyostelium/crecimiento & desarrollo , Animales , Diferenciación Celular , AMP Cíclico/fisiología , Dictyostelium/genética , Perfilación de la Expresión Génica , Genes Protozoarios/fisiologíaRESUMEN
We performed a screen for signaling genes by selecting mutant strains of Dictyostelium that fail to develop spores in a pure population but sporulate well in chimerae with wild type cells. We found 9 strains whose sporulation was induced up to 10 million-fold in chimerae. Most strains were also able to sporulate in chimerae with each other, but 2 pairs failed to do so, suggesting that the genes in each pair participate in the production of 1 signal. One of the pairs, comD and comB, is described in detail. Sequence analysis revealed that both genes encode putative membrane proteins. ComD is predicted to have 15 transmembrane domains, and ComB has a region of high similarity to the Rab family of small GTPases and 1 transmembrane domain. Similarities between the developmental regulation and cell-type specificity of the genes' expression, the terminal developmental morphology, and the expression pattern of cell-type specific markers in the mutants suggest that comD and comB participate in 1 signal production pathway. This idea is also supported by a high similarity between the global transcriptional profiles of the mutant strains. Differences between the mutant phenotypes late in development suggest that comD and comB participate in separate processes as well. comD has a cell-autonomous role in the specialization of a novel prespore cell type, whereas comB has a cell-autonomous role in prestalk A cell differentiation.