Regulatory gene interactions controlling discoidin lectin expression in <i>Dictyostelium discoideum</i>

Alexander, Stephen; Leone, S.; Ostermeyer, Elizabeth A.; Sydow, Lisa M.

doi:10.1002/dvg.1020110515

Cited by 14 publications

(16 citation statements)

References 21 publications

(5 reference statements)

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“…both growing and developing cells (1,4). This is in contrast to wild-type cells which first begin to accumulate discoidin during the aggregation phase of development.…”

Section: Resultsmentioning

confidence: 78%

“…In contrast, cAMP has been shown to be a negative regulator of discoidin gene transcription (34), since cAMP accumulation during development results in cessation of transcription of these genes. Recently, we have shown that cAMP, as well as folic acid, also negatively regulates discoidin lectin expression during growth of axenic cells (4 (31).…”

Section: Discussionmentioning

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).…”

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confidence: 99%

“…Taken (29). The genetic techniques and nomenclature used in this study were discussed in detail in the previous papers in this series (1,4 Southern blotting. Southern analysis of the discoidin lectin gene family has been described (6).…”

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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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“…both growing and developing cells (1,4). This is in contrast to wild-type cells which first begin to accumulate discoidin during the aggregation phase of development.…”

Section: Resultsmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

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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“…Alternatively, gdt1 may be in a parallel, interacting pathway. The idea that discoidin expression is controlled by a network of pathways was already proposed by Alexander et al (1986Alexander et al ( , 1990. It should be noted that the double mutant also shows that G␣2-mediated signaling apparently splits into two branches: although the GDT (i.e.…”

Section: Discussionmentioning

confidence: 80%

gdt1, a New Signal Transduction Component for Negative Regulation of the Growth–Differentiation Transition inDictyostelium discoideum

Zeng

Anjard

Riemann

et al. 2000

MBoC

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Discoidin I expression was used as a marker to screen for mutants affected in the growthdifferentiation transition (GDT) of Dictyostelium. By REMI mutagenesis we have isolated mutant 2-9, an overexpressor of discoidin I. It displays normal morphogenesis but shows premature entry into the developmental cycle. The disrupted gene was denominated gdt1. The mutant phenotype was reconstructed by disruptions in different parts of the gene, suggesting that all had a complete loss of function. gdt1 was expressed in growing cells; the levels of protein and mRNA appear to increase with cell density and rapidly decrease with the onset of development. gdt1 encodes a 175-kDa protein with four putative transmembrane domains. In the C terminus, the derived amino acid sequence displays some similarity to the catalytic domain of protein kinases. Mixing experiments demonstrate that the gdt1 Ϫ phenotype is cell autonomous. Prestarvation factor is secreted at wild-type levels. The response to folate, a negative regulator of discoidin expression, was not impaired in gdt1 mutants. Cells that lack the G protein ␣2 display a loss of discoidin expression and do not aggregate. gdt1 Ϫ /G␣2 Ϫ double mutants show no aggregation but strong discoidin expression. This suggests that gdt1 is a negative regulator of the GDT downstream of or in a parallel pathway to G␣2.

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Absence of complementation in non-allelic mutants of Dictyostelium discoideum with defects in the transition from growth to development

2001

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In Dictyostelium discoideum, growth and development are mutually exclusive and the transition between the two phases of the life cycle is regulated by the environment. This regulation is disturbed in HBW3, a chemically induced mutant with an unknown molecular defect. The mutant develops rapidly and expresses developmental markers during growth. Here we show that HBW3 fails to complement another mutant which has a similar phenotype: a targeted knock-out of the gdt1 gene. We further show that both mutations are recessive and that both are located on chromosome III, suggesting that the two mutations might be allelic. Molecular analysis, however, demonstrates that the gdt1 gene is not mutated in HBW3. Thus, although a wild-type copy of each gene is present in diploid cell lines, the defects due to the recessive mutations synergize to produce a detectable phenotype. The phenotypic similarities and differences between the two mutants are discussed.

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Regulatory gene interactions controlling discoidin lectin expression in Dictyostelium discoideum

Cited by 14 publications

References 21 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.

gdt1, a New Signal Transduction Component for Negative Regulation of the Growth–Differentiation Transition inDictyostelium discoideum

Absence of complementation in non-allelic mutants of Dictyostelium discoideum with defects in the transition from growth to development

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