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F Banuett

Publications and source records attributed to F Banuett.

14 recordsLinked to original sources
PubMed1998

Signalling in the yeasts: an informational cascade with links to the filamentous fungi.

All cells, from bacteria and yeasts to mammalian cells, respond to cues from their environment. A variety of mechanisms exist for the transduction of these external signals to the interior of the cell, resulting in altered patterns of protein activity. Eukaryotic cells commonly transduce external cues via a conserved module composed of three protein kinases, the mitogen-activated protein kinase (MAPK) cascade. This module can then activate substrates, some of which include transcriptional activators. Multiple MAPK signalling pathways coexist in a cell. This review considers different MAPK cascade signalling pathways that govern several aspects of the life cycle of budding and fission yeasts: conjugation and meiosis by the pheromone response pathway, stress response by the high-osmolarity sensing pathway, cell wall biosynthesis in response to activation of the low-osmolarity and heat-sensing pathway, and pseudohyphal growth in response to activation of a subset of the components of the pheromone response pathway. Because the MAPK cascade components are highly conserved, a key question in studies of these pathways is the mechanism by which specificity of response is achieved. Several other issues to be addressed in this review concern the nature of the receptors used to sense the external signals and the mechanism by which the receptors communicate with other components leading to activation of the MAPK cascade. Recently, it has become apparent that MAPK cascades are important in governing the pathogenicity of filamentous fungi.

Calcium-Calmodulin-Dependent Protein Kinases↗
PubMed1996

Discrete developmental stages during teliospore formation in the corn smut fungus, Ustilago maydis.

Ustilago maydis is a dimorphic fungus with a yeast-like non-pathogenic form and a filamentous (hyphal) pathogenic form that induces tumor formation in maize. Within mature tumors, hyphae give rise to teliospores, which are round, diploid cells surrounded by a specialized cell wall. Here we describe the time course of fungal development in the plant with a focus on the morphological changes in the hyphae and the pathway of teliospore formation. We confirm and extend earlier observations that U. maydis hyphae branch extensively on the leaf surface and intracellularly before induction of tumors. We observe that at later stages the filaments undergo a series of discrete morphogenetic changes leading to teliospore formation. In particular, we show that the hyphae become embedded in a mucilaginous matrix within the tumor cells and the hyphal tips become modified. The hyphae then undergo fragmentation to release individual cells that exhibit a variety of shapes on their way to becoming rounded. Finally, a specialized cell wall is deposited. Support for the existence of such a pathway comes from analysis of a mutant defective in the fuz1 gene: inactivation of fuz1 blocks production of the mucilaginous matrix and fragmentation of the hyphae, leading to a defect in teliospore formation. The different morphological changes that occur while in the plant but not in culture suggest that plant inputs play a key role in fungal development.

Gene Deletion↗
PubMed1995

Genetics of Ustilago maydis, a fungal pathogen that induces tumors in maize.

Ustilago maydis induces tumors in maize. It is dimorphic, with a unicellular, nonpathogenic form, and a dikaryotic, filamentous, pathogenic form that requires the plant for its growth. The life cycle is regulated by two mating type loci, a and b: a has two alleles, which encode a pheromone and a receptor; b is multiallelic and encodes a combinatorial homeodomain protein. Cell fusion occurs between haploid cells with different a alleles. The dikaryon formed exhibits filamentous growth if the cells also carry any two different b alleles. The b locus is the major pathogenicity determinant, fuz7, which encodes a MAP kinase activator, is also necessary for tumor induction and may respond to plant signals. Several other genes have been identified (fuz1, fuz2, rtf1, uac, ubc) that affect different aspects of the life cycle transitions. Some of them may identify targets of the b locus. Signaling between pathogen and plant is of key importance in tumor induction and fungal growth and differentiation within the plant. The role of siderophores is also discussed.

Genes, Fungal↗
PubMed1994

Identification of fuz7, a Ustilago maydis MEK/MAPKK homolog required for a-locus-dependent and -independent steps in the fungal life cycle.

Ustilago maydis is a plant pathogenic Basidiomycete fungus that exhibits dimorphism--it has a haploid, yeast-like phase and a dikaryotic, filamentous phase that is pathogenic. Establishment and maintenance of these two forms are controlled by two mating type loci, a and b. The a locus is thought to govern fusion of haploid cells to form a dikaryon and is also required for filamentous growth of the dikaryon. It encodes two components of a pheromone response pathway: pheromones and receptors. We report the identification of the U. maydis fuz7 gene, which codes for a putative dual specificity serine/threonine tyrosine kinase of the MAP kinase kinase (MAPKK/MEK) family, by homology with other members of the family. Analysis of mutants deleted for fuz7 shows that it participates in different facets of the life cycle: It is necessary for a-locus-dependent processes, such as conjugation tube formation, filament formation, and maintenance of filamentous growth, and for a-locus-independent processes, such as tumor induction and teliospore germination. fuz7 is the first U. maydis gene distinct from the b locus required for fungal pathogenicity. We propose that fuz7 is involved in at least two pathways, one of which responds to the pheromones coded by the a locus and the other to putative signals from the plant.

Amino Acid Sequence↗
PubMed1993

The Escherichia coli hflA locus encodes a putative GTP-binding protein and two membrane proteins, one of which contains a protease-like domain.

The hflA (high frequency of lysogenization) locus of Escherichia coli governs the lysis-lysogeny decision of bacteriophage lambda by controlling stability of the phage cII protein. hflA contains three genes, hflX, hflK, and hflC, encoding polypeptides of 50, 46, and 37 kDa, respectively. We have determined the nucleotide sequence of 3843 base pairs containing hflA and have found three large open reading frames corresponding to hflX, hflK, and hflC. HflX contains the three sequence motifs typical of GTP-binding proteins and appears to be a member of a distinct family of putative GTPases. HflC and HflK appear to be integral membrane proteins which show some similarity to each other and to a human membrane protein. The C-terminal region of HflC contains a domain resembling the catalytic domain of ClpP, a bacterial ATP-dependent protease. We hypothesize that HflK and HflC constitute a distinct membrane-bound protease whose activity may be modulated by HflX GTPase.

Adenosine Triphosphate↗
PubMed1992

Ustilago maydis, the delightful blight.

Recent studies of the corn smut fungus life cycle and its regulation by two mating type loci and other genes provide a cornucopia of challenges in cell biology, genetics and protein structure. The fungus can exist in two states: nonpathogenic and pathogenic. The change from one state to the other is accompanied by a change in morphology (yeast-like to filamentous) and growth properties (saprophytic to parasitic).

Amino Acid Sequence↗
PubMed1991

Identification of genes governing filamentous growth and tumor induction by the plant pathogen Ustilago maydis.

Two master regulatory loci, a and b, govern life-cycle transitions of the phytopathogenic fungus Ustilago maydis. Fusion of haploids that differ at both a and b results in production of a filamentous dikaryon, which induces tumors in its host, maize. Here I describe identification of genes distinct from a and b that play roles in these life-cycle transitions. These studies identify three genes, fuz1, fuz2, and rtf1, that are necessary for filament formation. fuz1 is also necessary for normal size and distribution of tumors and for teliospore formation; fuz2 is also necessary for teliospore germination. Mutations in the rtf1 gene, which are recessive, bypass the requirement of different b alleles for tumor formation. This observation indicates that rtf1 codes for a negative regulator of tumor induction. The fuz1, fuz2, and rtf1 genes may be targets for the a and b loci.

Alleles↗
PubMed1990

The b alleles of U. maydis, whose combinations program pathogenic development, code for polypeptides containing a homeodomain-related motif.

U. maydis is a fungal pathogen of corn with two forms: one is yeast-like and nonpathogenic; the other is filamentous and pathogenic. The b locus, with 25 different alleles, regulates this dimorphism: any combination of two different alleles triggers pathogenic development, whereas the presence of identical alleles results in the yeast-like form. We have cloned four b alleles (b1, b2, b3, and b4) and show that the b locus contains a single open reading frame (ORF) of 410 amino acids with a variable N-terminal region and a highly conserved C-terminal region (60% and 93% identity, respectively). Mutational analysis confirms that this ORF is responsible for b activity. The b polypeptides appear to be DNA binding proteins because they contain a motif related to the homeodomain in their constant region. We propose that combinatorial interactions between b polypeptides generate regulatory proteins that determine the developmental program of the fungus.

Alleles↗
PubMed1989

Different a alleles of Ustilago maydis are necessary for maintenance of filamentous growth but not for meiosis.

Two loci (the incompatibility or mating type loci), a and b, govern the life cycle of Ustilago maydis, a fungal pathogen of corn. U. maydis diploids heterozygous at both a and b (a[unk] b[unk]) form mycelial colonies (Fuz(+) phenotype), induce tumors, and produce teliospores able to undergo meiosis. We report here the isolation and characterization of nonmycelial (Fuz(-)) derivatives. These Fuz(-) diploids have allowed us to examine the requirement of a[unk] and b[unk] in maintenance of filamentous growth and tumor-inducing ability. The Fuz(-) diploids are of four classes: two are inferred to be homozygous for b (a[unk] b=); the other two are shown to be homozygous for a (a= b[unk]). These observations confirm the requirement for b[unk] and reveal the requirement for a[unk] in filamentous growth. U. maydis is thus like other basidiomycetes that have two loci governing growth of the dikaryotic filament. The mating behavior of the Fuz(-) diploids indicates that heterozygosity at a or b does not block mating. Although both a= b[unk] and a[unk] b= diploids are nonmycelial, they differ in that a[unk] b= diploids are nonpathogenic, whereas a= b[unk] diploids are pathogenic and produce teliospores able to undergo meiosis. These findings substantiate previous, more limited observations. They demonstrate that ability to induce tumors and produce normal teliospores requires different alleles at b but not at a.

Journal Article↗
PubMed1987

Identification of polypeptides encoded by an Escherichia coli locus (hflA) that governs the lysis-lysogeny decision of bacteriophage lambda.

We report the cloning of the Escherichia coli hflA locus, which governs stability of phage lambda cII protein and which has been proposed to encode or regulate a cII-specific protease. The hflA locus was cloned on an 18-kilobase DNA fragment by selecting for plasmids that carry the neighboring purA gene. The boundaries of hflA were delimited by analysis of deletions and insertions constructed in vitro and by use of transposon Tn1000. Maxicell analysis of the proteins encoded by the hflA-containing fragment shows that hflA consists of at least two nonoverlapping genes, hflC and hflK, encoding polypeptides of 37,000 (C) and 46,000 (K) daltons. We observe that insertions into one gene eliminate the corresponding polypeptide and greatly reduce synthesis of the other. We suggest that these two polypeptides (K and C) interact to form a multimeric complex and that free subunits are unstable. We have constructed two types of fusions between hflA and lacZ. One is an hflC-lacZ protein fusion constructed in vitro; the other is an hfl-lacZ operon fusion in which a Mu dX(Apr lac) has inserted into the hflK gene. We have used the operon fusion to infer the direction of transcription of the hflK gene--toward hflC and in the same direction as hflC. Last, we describe evidence that hflA contains an additional gene, hflX, encoding a 50,000-dalton polypeptide.

Autoradiography↗
PubMed1986

hflB, a new Escherichia coli locus regulating lysogeny and the level of bacteriophage lambda cII protein.

The level of the viral cII protein has been proposed to be the crucial determinant in the lysis-lysogeny decision of bacteriophage lambda. A new Escherichia coli locus (hflB) has been identified in which a mutation (hflB29) leads to high frequency of lysogeny by lambda. A double mutant defective in both hflB and the previously identified hflA gene displays a more severe Hfl- phenotype than either single mutant. The hflB locus is at 69 minutes on the E. coli map, 85% co-transducible with argG. The hflB29 mutation results in increased stability of the phage cII protein (increasing its half-life twofold) and is recessive to hflB+. We conclude that the hflB+ locus is a negative regulator of cII, perhaps coding for or regulating a protease that acts on cII. In addition, we observe that the can1 mutation, an alteration of the cII gene that results in enhanced lysogenization, leads to increased stability of cII protein. These observations reinforce the view that the level of cII is a key factor in the lysis-lysogeny decision of lambda.

Bacteriophage lambda↗