Multiple regulatory genes control expression of a gene family during development of Dictyostelium discoideum.

Alexander, Stephen; Cibulsky, A M; Cuneo, Susan D.

doi:10.1128/mcb.6.12.4353

Cited by 11 publications

(21 citation statements)

References 40 publications

(36 reference statements)

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“…The defects in these strains were shown to be at the level of transcription and specific to the discoidin genes (5). Genetic studies indicate that the mutations define a network of trans-acting regulatory genes (1). Each mutation maps to a different chromosome.…”

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confidence: 99%

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Translational control of discoidin lectin expression in drsA suppressor mutants of Dictyostelium discoideum.

Alexander¹,

Leone²,

Ostermeyer³

1991

Mol. Cell. Biol.

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Genetic analysis in Dictyostelium discoideum has identified regulatory genes which control the developmental expression of the discoidin lectin multigene family. Among these, the drsA mutation is a dominant second-site suppressor of another mutation, disB, which has the discoidinless phenotype. We now demonstrate a novel mechanism by which the drsA allele exerts its suppressive effect on the disB mutation. Interestingly, drsA does not merely bypass the disB mutation and restore the wild-type pattern of lectin expression. Rather, drsA mutant cells have high levels of discoidin lectin synthesis during growth but do not express lectins during aggregation. In contrast, wild-type cells only express lectin protein during the aggregation period of development. Phenocopies of the drsA mutation show a pattern of discoidin expression similar to that seen in the bona fide mutant. These data suggest that there may be a mechanism of negative feedback, resulting from the high levels of discoidin lectin made during growth, which inhibits further discoidin lectin expression during development. Northern (RNA) analysis of developing drsA mutant cells shows that these cells contain high levels of discoidin mRNA, although no discoidin lectin protein is being translated from these messages. Therefore, expression of the discoidin gene family can be controlled at the level of translation as well as transcription.

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confidence: 99%

“…In contrast, drsA does not suppress the disA mutation, and cells containing both of these mutations do not express the discoidin lectins. The epistatic relationship of these genes allowed us to propose a model for the gene action sequence: disB+-->drsA+-*disA+ (1,4).…”

mentioning

confidence: 99%

Translational control of discoidin lectin expression in drsA suppressor mutants of Dictyostelium discoideum.

Alexander¹,

Leone²,

Ostermeyer³

1991

Mol. Cell. Biol.

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“…As shown in Fig. 3, the catA null strain IR29 is extremely sensitive to H # O # -even more so than Garcia Alexander et al (1986) et al (2000) observed for X9 -consistent with a more severe phenotype. At low concentrations of H # O # , which barely affect the parental strain, IR29 cells are nearly all killed ("90 % at 0n1 mM; "99n9 % at 0n3 mM).…”

Section: Phenotypes Of Cata Disruption Mutantsmentioning

confidence: 86%

“…Forward mutations to methanol resistance have also been used as a simple mutation assay for testing the effects of different DNA-damaging agents (Podgorski & Deering, 1980). Although many methanol-resistant Dictyostelium strains have been generated previously (Alexander et al, 1986 ;Rothman & Alexander, 1975 ;Williams et al, 1974), the molecular basis for resistance to methanol in Dictyostelium cells remained unknown. In this study we used REMI to identify mutations that were responsible for methanol resistance and demonstrated that the acrA locus contains the catA gene.…”

Section: Discussionmentioning

confidence: 99%

“…These drug-resistance mutations have been essential in genetic mapping in Dictyostelium (Alexander et al, 1986 ;Welker & Deering, 1976) and in integrating the genetic and physical maps of the Dictyostelium linkage groups (Loomis et al, 1995). However, the structural gene encoded by acrA has remained unknown for the past 25 years.…”

Section: Ma X U Garcia and C Roberts Contributed Equally To This mentioning

confidence: 99%

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Methanol and acriflavine resistance in Dictyostelium are caused by loss of catalase The GenBank accession number for the sequence reported in this paper is AF090443.

et al. 2002

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Various chemicals with harmful effects are not themselves toxic, but are metabolized in vivo to produce toxic products. One example is methanol in Dictyostelium, which is lethal to cells containing the acrA gene, but relatively harmless to acrA mutants. This makes methanol resistance one of the tightest genetic selections in Dictyostelium. Loss of acrA also confers cross-resistance to unrelated compounds such as acriflavine and thiabendazole. We have used insertional mutagenesis to demonstrate that the acrA locus encodes the peroxisomal catalase A enzyme. Disruption of the catA gene results in parallel resistance to acriflavine. Molecular and biochemical studies of several previously characterized methanol-resistant strains reveal that each lacks catalase activity. One allele, acrA2, contains a 13 bp deletion which introduces a frameshift in the middle of the gene. The involvement of catalase in methanol resistance in Dictyostelium compares with its role in methanol metabolism in yeast and rodents. However, this is the first study to show that catalase is required for the toxicity of acriflavine. Our results imply that acriflavine and thiabendazole are precursors which must be oxidized to generate biologically active species. The catA/acrA gene is also a potentially invaluable negative selectable marker for Dictyostelium molecular genetics.

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Regulatory gene interactions controlling discoidin lectin expression in Dictyostelium discoideum

et al. 1990

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Genetic studies have revealed a network of three unlinked regulatory genes that control the developmental expression of the family of endogenous lectins in Dictyosteliurn discoideurn.Mutations in the disA and dis5 loci have a null phenotype and do not express the discoidin I or I I lectins. The third mutation, drsA, is a second-site suppressor of the dis5 mutation, which restores expression of all lectin species. Cells carrying this mutation express the discoidin lectins during growth, which is in contrast to wild-type cells in which lectin synthesis is developmentally regulated. In addition to this basic level of genetic control, the conditions of growth dramatically influence the patterns of discoidin expression. Growth-phase wild-type cells do not express lectin if the cells are grown on plates in association with bacteria. However, wild-type cells growing in bacterial suspensions express high levels of lectin during growth. Synthesis of the discoidin lectins in growing cells is sensitive to the levels of extracellular cyclic adenosine monophosphate (CAMP) and folic acid. These results suggest that the drsA mutation renders cells insensitive to cAMP and/or folate and thus allows expression of lectin during growth.

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Multiple regulatory genes control expression of a gene family during development of Dictyostelium discoideum.

Cited by 11 publications

References 40 publications

Translational control of discoidin lectin expression in drsA suppressor mutants of Dictyostelium discoideum.

Translational control of discoidin lectin expression in drsA suppressor mutants of Dictyostelium discoideum.

Methanol and acriflavine resistance in Dictyostelium are caused by loss of catalase The GenBank accession number for the sequence reported in this paper is AF090443.

Regulatory gene interactions controlling discoidin lectin expression in Dictyostelium discoideum

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