Septum formation in Aspergillus nidulans

1995 ◽  
Vol 73 (S1) ◽  
pp. 396-399 ◽  
Author(s):  
Michelle Momany ◽  
Jennifer L. Morrell ◽  
Steven D. Harris ◽  
John E. Hamer
Keyword(s):  
Aspergillus Nidulans ◽  
Antibody Production ◽  
Nuclear Division ◽  
Temperature Sensitive ◽  
Cellular Processes ◽  
The Third ◽  
Septum Formation ◽  
Chromosome Transmission ◽  
Insight Into

We are investigating septation in Aspergillus nidulans. We have shown that septum formation is dependent on the third nuclear division and actin is involved in this process. We have also characterized nine temperature-sensitive septation (sep) mutants. On the basis of our analysis we have divided these mutants into three phenotypic classes. We are uncovering the order of events in the septation pathway by analysis of double mutants constructed with different pairs of sep mutants. The sepB gene has been cloned and sequenced. Homology with the Saccharomyces cerevisiae CTF4 gene and the phenotype of the sepB mutant support a role in monitoring the fidelity of chromosome transmission. We are also investigating the role of the asp genes (Aspergillus septins). Three asp genes were identified by homology with the S. cerevisiae septins. aspB has been cloned, sequenced, and fused to a biotinylated tag for antibody production. Antibody production and localization studies are now underway. Because septation requires the integration of several cellular processes, our studies should give insight into the cell cycle, cell wall biosnythesis and development of A. nidulans. Key words: septation, cytokinesis, Aspergillus nidulans.

scholarly journals Identification and characterization of Aspergillus nidulans mutants defective in cytokinesis.

Genetics ◽  
1994 ◽  
Vol 136 (2) ◽  
pp. 517-532 ◽  
Author(s):  
S D Harris ◽  
J L Morrell ◽  
J E Hamer
Keyword(s):  
Aspergillus Nidulans ◽  
Nuclear Division ◽  
Temperature Shift ◽  
Mitotic Division ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
The Third ◽  
Septum Formation ◽  
New Genes

Abstract Filamentous fungi undergo cytokinesis by forming crosswalls termed septa. Here, we describe the genetic and physiological controls governing septation in Aspergillus nidulans. Germinating conidia do not form septa until the completion of their third nuclear division. The first septum is invariantly positioned at the basal end of the germ tube. Block-and-release experiments of nuclear division with benomyl or hydroxyurea, and analysis of various nuclear division mutants demonstrated that septum formation is dependent upon the third mitotic division. Block-and-release experiments with cytochalasin A and the localization of actin in germlings by indirect immunofluorescence showed that actin participated in septum formation. In addition to being concentrated at the growing hyphal tips, a band of actin was also apparent at the site of septum formation. Previous genetic analysis in A. nidulans identified four genes involved in septation (sepA-D). We have screened a new collection of temperature sensitive (ts) mutants of A. nidulans for strains that failed to form septa at the restrictive temperature but were able to complete early nuclear divisions. We identified five new genes designated sepE, G, H, I and J, along with one additional allele of a previously identified septation gene. On the basis of temperature shift experiments, nuclear counts and cell morphology, we sorted these cytokines mutants into three phenotypic classes. Interestingly, one class of mutants fails to form septa and fails to progress past the third nuclear division. This class of mutants suggests the existence of a regulatory mechanism in A. nidulans that ensures the continuation of nuclear division following the initiation of cytokinesis.

Cytokinesis in Aspergillus nidulans is controlled by cell size, nuclear positioning and mitosis

1996 ◽  
Vol 109 (8) ◽  
pp. 2179-2188 ◽  
Author(s):  
T.D. Wolkow ◽  
S.D. Harris ◽  
J.E. Hamer
Keyword(s):  
Aspergillus Nidulans ◽  
Cell Size ◽  
Nuclear Division ◽  
Size Control ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
Nuclear Positioning ◽  
Septum Formation ◽  
Nuclear Distribution ◽  
Cellular Compartments

The mycelium of Aspergillus nidulans is composed of multinucleate cellular compartments delimited by crosswalls called septa. Septum formation is dependent on mitosis and requires the recruitment of actin to the site of septum formation. Employing a collection of temperature sensitive nuclear distribution (nudA2, nudC3 and nudF7), nuclear division (nimA5, hfaB3), and septation (sepD5, sepG1) mutants, we have investigated the interdependency among nuclear positioning, mitosis, and cell growth in structuring the cellular compartments of A. nidulans. The cellular compartments of nud+ strains were highly uniform with regard to nuclear distribution and averaged 38 microns in length. Incubation of nud mutants at semi-restrictive temperature resulted in aberrant nuclear distribution that appeared to direct the formation of variable-sized cellular compartments, ranging from 5 microns to greater than 81 microns. In germinating spores, the first septum forms at the basal end of the germ tube following the third round of nuclear division. Germlings must undergo mitosis in order to form a septum. Temperature-sensitive mitotic mutants were used to show that a single nuclear division is sufficient to activate septum formation, provided a critical cell size has been attained. In mitotic mutants and wild-type cells, delays in nuclear division resulted in the misplacement of the first septum. These results strongly support the role of mitotic nuclei in determining septal placement, and suggest that cell size control is post-mitotic in A. nidulans.

Extragenic Suppressors of thenimX2cdc2Mutation ofAspergillus nidulansAffect Nuclear Division, Septation and Conidiation

Genetics ◽  
2000 ◽  
Vol 156 (4) ◽  
pp. 1573-1584
Author(s):  
Sarah Lea McGuire ◽  
Dana L Roe ◽  
Brett W Carter ◽  
Robert L Carter ◽  
Sean P Grace ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Aspergillus Nidulans ◽  
Biochemical Analysis ◽  
Nuclear Division ◽  
Temperature Sensitive ◽  
Suppressor Genes ◽  
Suppressor Mutations ◽  
Cold Sensitive ◽  
Extragenic Suppressors

AbstractThe Aspergillus nidulans NIMXCDC2 protein kinase has been shown to be required for both the G2/M and G1/S transitions, and recent evidence has implicated a role for NIMXCDC2 in septation and conidiation. While much is understood of its G2/M function, little is known about the functions of NIMXCDC2 during G1/S, septation, and conidiophore development. In an attempt to better understand how NIMXCDC2 is involved in these processes, we have isolated four extragenic suppressors of the A. nidulans nimX2cdc2 temperature-sensitive mutation. Mutation of these suppressor genes, designated snxA-snxD for suppressor of nimX, affects nuclear division, septation, and conidiation. The cold-sensitive snxA1 mutation leads to arrest of nuclear division during G1 or early S. snxB1 causes hyperseptation in the hyphae and sensitivity to hydroxyurea, while snxC1 causes septation in the conidiophore stalk and aberrant conidiophore structure. snxD1 leads to slight septation defects and hydroxyurea sensitivity. The additional phenotypes that result from the suppressor mutations provide genetic evidence that NIMXCDC2 affects septation and conidiation in addition to nuclear division, and cloning and biochemical analysis of these will allow a better understanding of the role of NIMXCDC2 in these processes.

Regulation of Septum Formation in Aspergillus nidulans by a DNA Damage Checkpoint Pathway

Genetics ◽  
1998 ◽  
Vol 148 (3) ◽  
pp. 1055-1067
Author(s):  
Steven D Harris ◽  
Peter R Kraus
Keyword(s):  
Dna Damage ◽  
Aspergillus Nidulans ◽  
Cellular Response ◽  
Dna Damage Checkpoint ◽  
Temperature Sensitive ◽  
Dna Metabolism ◽  
Chromosomal Dna ◽  
Checkpoint Response ◽  
Septum Formation ◽  
Checkpoint Pathway

Abstract In Aspergillus nidulans, germinating conidia undergo multiple rounds of nuclear division before the formation of the first septum. Previous characterization of temperature-sensitive sepB and sepJ mutations showed that although they block septation, they also cause moderate defects in chromosomal DNA metabolism. Results presented here demonstrate that a variety of other perturbations of chromosomal DNA metabolism also delay septum formation, suggesting that this is a general cellular response to the presence of sublethal DNA damage. Genetic evidence is provided that suggests that high levels of cyclin-dependent kinase (cdk) activity are required for septation in A. nidulans. Consistent with this notion, the inhibition of septum formation triggered by defects in chromosomal DNA metabolism depends upon Tyr-15 phosphorylation of the mitotic cdk p34nimX. Moreover, this response also requires elements of the DNA damage checkpoint pathway. A model is proposed that suggests that the DNA damage checkpoint response represents one of multiple sensory inputs that modulates p34nimX activity to control the timing of septum formation.

scholarly journals A High Copy Suppressor Screen Reveals Genetic Interactions Between BET3 and a New Gene: Evidence for a Novel Complex in ER-to-Golgi Transport

Genetics ◽  
1998 ◽  
Vol 149 (2) ◽  
pp. 833-841
Author(s):  
Yu Jiang ◽  
Al Scarpa ◽  
Li Zhang ◽  
Shelly Stone ◽  
Ed Feliciano ◽  
...  
Keyword(s):  
Growth Defect ◽  
Carboxypeptidase Y ◽  
Temperature Sensitive ◽  
Yeast Saccharomyces Cerevisiae ◽  
Specific Suppression ◽  
Golgi Transport ◽  
New Gene ◽  
Insight Into ◽  
Suppressor Screen

Abstract The BET3 gene in the yeast Saccharomyces cerevisiae encodes a 22-kD hydrophilic protein that is required for vesicular transport between the ER and Golgi complex. To gain insight into the role of Bet3p, we screened for genes that suppress the growth defect of the temperature-sensitive bet3 mutant at 34°. This high copy suppressor screen resulted in the isolation of a new gene, called BET5. BET5 encodes an essential 18-kD hydrophilic protein that in high copy allows growth of the bet3-1 mutant, but not other ER accumulating mutants. This strong and specific suppression is consistent with the fact that Bet3p and Bet5p are members of the same complex. Using PCR mutagenesis, we generated a temperature-sensitive mutation in BET5 (bet5-1) that blocks the transport of carboxypeptidase Y to the vacuole and prevents secretion of the yeast pheromone α-factor at 37°. The precursor forms of these proteins that accumulate in this mutant are indicative of a block in membrane traffic between the ER and Golgi apparatus. High copy suppressors of the bet5-1 mutant include several genes whose products are required for ER-to-Golgi transport (BET1, SEC22, USO1 and DSS4) and the maintenance of the Golgi (ANP1). These findings support the hypothesis that Bet5p acts in conjunction with Bet3p to mediate a late stage in ER-to-Golgi transport. The identification of mammalian homologues of Bet3p and Bet5p implies that the Bet3p/Bet5p complex is highly conserved in evolution.

scholarly journals GlcNAcstatins are nanomolar inhibitors of human O-GlcNAcase inducing cellular hyper-O-GlcNAcylation

2009 ◽  
Vol 420 (2) ◽  
pp. 221-227 ◽  
Author(s):  
Helge C. Dorfmueller ◽  
Vladimir S. Borodkin ◽  
Marianne Schimpl ◽  
Daan M. F. van Aalten
Keyword(s):  
Active Site ◽  
Cell Biology ◽  
Rational Design ◽  
Catalytic Mechanism ◽  
Conserved Residues ◽  
Cellular Processes ◽  
Acetyl Group ◽  
Nanomolar Range ◽  
Insight Into

O-GlcNAcylation is an essential, dynamic and inducible post-translational glycosylation of cytosolic proteins in metazoa and can show interplay with protein phosphorylation. Inhibition of OGA (O-GlcNAcase), the enzyme that removes O-GlcNAc from O-GlcNAcylated proteins, is a useful strategy to probe the role of this modification in a range of cellular processes. In the present study, we report the rational design and evaluation of GlcNAcstatins, a family of potent, competitive and selective inhibitors of human OGA. Kinetic experiments with recombinant human OGA reveal that the GlcNAcstatins are the most potent human OGA inhibitors reported to date, inhibiting the enzyme in the sub-nanomolar to nanomolar range. Modification of the GlcNAcstatin N-acetyl group leads to up to 160-fold selectivity against the human lysosomal hexosaminidases which employ a similar substrate-assisted catalytic mechanism. Mutagenesis studies in a bacterial OGA, guided by the structure of a GlcNAcstatin complex, provides insight into the role of conserved residues in the human OGA active site. GlcNAcstatins are cell-permeant and, at low nanomolar concentrations, effectively modulate intracellular O-GlcNAc levels through inhibition of OGA, in a range of human cell lines. Thus these compounds are potent selective tools to study the cell biology of O-GlcNAc.

Sebastian Moore’s Spiritual Vision and Christological Project

2018 ◽  
Vol 136 (3) ◽  
pp. 165-177
Author(s):  
Louis Roy OP
Keyword(s):  
Structural Components ◽  
The Third ◽  
Insight Into

This essay wants to examine the structural components and the viability of Sebastian Moore’s christological construction. The first section presents the origin of his insight into the redemptive role of Jesus. The second section reports his views on desire. In connection with desire, the third section details the experience that the followers of Jesus had of him, from the beginnings in Galilee, through his passion and death, ending with his appearances after his resurrection. The fourth justifies the validity of his Christology.

scholarly journals A novel histone H4 mutant defective in nuclear division and mitotic chromosome transmission.

1996 ◽  
Vol 16 (3) ◽  
pp. 1017-1026 ◽  
Author(s):  
M M Smith ◽  
P Yang ◽  
M S Santisteban ◽  
P W Boone ◽  
A T Goldstein ◽  
...  
Keyword(s):  
Mitotic Chromosome ◽  
Nuclear Division ◽  
Dna Recombination ◽  
Chromosome Loss ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
Histone H4 ◽  
Eukaryotic Chromosome ◽  
Chromosome Transmission

The histone proteins are essential for the assembly and function of th e eukaryotic chromosome. Here we report the first isolation of a temperature-sensitive lethal histone H4 mutant defective in mitotic chromosome transmission Saccharomyces cerevisiae. The mutant requires two amino acid substitutions in histone H4: a lethal Thr-to-Ile change at position 82, which lies within one of the DNA-binding surfaces of the protein, and a substitution of Ala to Val at position 89 that is an intragenic suppressor. Genetic and biochemical evidence shows that the mutant histone H4 is temperature sensitive for function but not for synthesis, deposition, or stability. The chromatin structure of 2 micrometer circle minichromosomes is temperature sensitive in vivo, consistent with a defect in H4-DNA interactions. The mutant also has defects in transcription, displaying weak Spt- phenotypes. At the restrictive temperature, mutant cells arrest in the cell cycle at nuclear division, with a large bud, a single nucleus with 2C DNA content, and a short bipolar spindle. At semipermissive temperatures, the frequency of chromosome loss is elevated 60-fold in the mutant while DNA recombination frequencies are unaffected. High-copy CSE4, encoding an H3 variant related to the mammalian CENP-A kinetochore antigen, was found to suppress the temperature sensitivity of the mutant without suppressing the Spt- transcription defect. These genetic, biochemical, and phenotypic results indicate that this novel histone H4 mutant defines one or more chromatin-dependent steps in chromosome segregation.

scholarly journals Cell division in Aspergillus

1992 ◽  
Vol 103 (3) ◽  
pp. 599-611 ◽  
Author(s):  
J.H. Doonan
Keyword(s):  
Cell Division ◽  
Aspergillus Nidulans ◽  
Molecular Analysis ◽  
Filamentous Fungus ◽  
Nuclear Division ◽  
Mutational Analysis ◽  
Cytoskeletal Proteins ◽  
Nuclear Movement ◽  
Cellular Analysis

Amenable to sophisticated genetic and molecular analysis, the simple filamentous fungus Aspergillus nidulans has provided some novel insights into the mechanisms and regulation of cell division. Mutational analysis has identified over fifty genes necessary for nuclear division, nuclear movement and cytokinesis. Molecular and cellular analysis of these mutants has led to the discovery of novel components of the cytoskeleton as well as to clarifying the role of established cytoskeletal proteins. Mutations leading to defects in the kinases (i.e. p34cdc2) and phosphatases (i.e. cdc25 and PP1), which are known to regulate mitosis in other eukaryotes, have been identified in Aspergillus. Additional, as yet novel, mitotic regulatory molecules, encoded by the nimA and bimE genes, have also been discovered in Aspergillus.

An Insight Into Mitochondrial Dysfunction and its Implications in Neuro-logical Diseases

2020 ◽  
Vol 22 ◽  
Author(s):  
Asimul Islam ◽  
Anas Shamsi ◽  
Rashid Waseem ◽  
Syed Kazim
Keyword(s):  
Mitochondrial Dysfunction ◽  
Neurodegenerative Disorders ◽  
Large Body ◽  
Ros Generation ◽  
Cell Organelles ◽  
Ischemic Brain ◽  
Cellular Processes ◽  
Vital Cell ◽  
Insight Into

Abstract:: In the last few years, a massive increase in the research has been observed that focusses on investigating the role of mitochondria in pathogenesis of several neurodegenerative disorders. Mitochondria are vital cell organelles having im-portant roles in different cellular processes including energy production, calcium signaling, ROS generation, apoptosis, etc. Therefore, healthy mitochondria are necessary for cell survival and functioning. It would seem feasible that mitochondrial dysfunction will have implications in various pathological conditions. A large body of evidence indicates the role of mito-chondrion as a potential key player in the loss or dysfunction of neurons in various neurodegenerative disorders. In this review, we provide an insight into the mitochondrial dysfunction and its involvement in the pathology of several neurolog-ical diseases such as Alzheimer’s disease, Parkinson’s disease, Amyotrophic Lateral Sclerosis, Hypoxic-Ischemic Brain Injury and many more.

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