Irniger, Stefan

[["dc.bibliographiccitation.firstpage","1278"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Molecular Microbiology"],["dc.bibliographiccitation.lastpage","1295"],["dc.bibliographiccitation.volume","71"],["dc.contributor.author","Bayram, Oezguer"],["dc.contributor.author","Sari, Fatih"],["dc.contributor.author","Braus, Gerhard H."],["dc.contributor.author","Irniger, Stefan"],["dc.date.accessioned","2018-11-07T08:32:21Z"],["dc.date.available","2018-11-07T08:32:21Z"],["dc.date.issued","2009"],["dc.description.abstract","Spore formation is a common process in the developmental cycle of fungi. In the yeast Saccharomyces cerevisiae, Ime2 is a key protein kinase for the meiotic cell cycle, which precedes ascospore formation. Here, we analysed the IME2-related imeB gene of the filamentous ascomycete Aspergillus nidulans. imeB deletion strains are retarded in growth and overproduce fertile sexual fruiting bodies in the presence of light, which normally represses sexual development. imeB mutants also display abnormal differentiation of sexual Hulle cells in submerged cultures. Increased sexual development of imeB mutants is dependent on VeA, a component of the heterotrimeric velvet complex. A combined deletion of imeB with the phytochrome fphA, a red light receptor, results in a complete loss of light response, suggesting that ImeB and FphA cooperate in light-mediated inhibition of sexual development. Furthermore, we found that imeB mutants fail to produce the mycotoxin sterigmatocystin, an aflatoxin precursor, and show that ImeB is needed for expression of the sterigmatocystin gene cluster. ImeB contains a TXY motif conserved in mitogen-activated protein kinases. This sequence element is essential for ImeB function. We conclude that ImeB is a mitogen-activated protein kinase-related protein kinase required for the co-ordinated control of light-dependent development with mycotoxin production."],["dc.identifier.doi","10.1111/j.1365-2958.2009.06606.x"],["dc.identifier.isi","000263522000017"],["dc.identifier.pmid","19210625"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17324"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.relation.issn","0950-382X"],["dc.title","The protein kinase ImeB is required for light-mediated inhibition of sexual development and for mycotoxin production in Aspergillus nidulans"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e1001226"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PLoS Genetics"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Bayram, Oezlem Sarikaya"],["dc.contributor.author","Bayram, Oezguer"],["dc.contributor.author","Valerius, Oliver"],["dc.contributor.author","Park, Hee Soo"],["dc.contributor.author","Irniger, Stefan"],["dc.contributor.author","Gerke, Jennifer"],["dc.contributor.author","Ni, Min"],["dc.contributor.author","Han, Kap-Hoon"],["dc.contributor.author","Yu, Jae-Hyuk"],["dc.contributor.author","Braus, Gerhard H."],["dc.date.accessioned","2018-11-07T08:36:31Z"],["dc.date.available","2018-11-07T08:36:31Z"],["dc.date.issued","2010"],["dc.description.abstract","VeA is the founding member of the velvet superfamily of fungal regulatory proteins. This protein is involved in light response and coordinates sexual reproduction and secondary metabolism in Aspergillus nidulans. In the dark, VeA bridges VelB and LaeA to form the VelB-VeA-LaeA (velvet) complex. The VeA-like protein VelB is another developmental regulator, and LaeA has been known as global regulator of secondary metabolism. In this study, we show that VelB forms a second light-regulated developmental complex together with VosA, another member of the velvet family, which represses asexual development. LaeA plays a key role, not only in secondary metabolism, but also in directing formation of the VelB-VosA and VelB-VeA-LaeA complexes. LaeA controls VeA modification and protein levels and possesses additional developmental functions. The laeA null mutant results in constitutive sexual differentiation, indicating that LaeA plays a pivotal role in inhibiting sexual development in response to light. Moreover, the absence of LaeA results in the formation of significantly smaller fruiting bodies. This is due to the lack of a specific globose cell type (Hulle cells), which nurse the young fruiting body during development. This suggests that LaeA controls Hulle cells. In summary, LaeA plays a dynamic role in fungal morphological and chemical development, and it controls expression, interactions, and modification of the velvet regulators."],["dc.identifier.doi","10.1371/journal.pgen.1001226"],["dc.identifier.isi","000285578900004"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7265"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18331"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1553-7404"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","LaeA Control of Velvet Family Regulatory Proteins for Light-Dependent Development and Fungal Cell-Type Specificity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2611"],["dc.bibliographiccitation.issue","13"],["dc.bibliographiccitation.journal","Cell Cycle"],["dc.bibliographiccitation.lastpage","2619"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Kuczera, Tanja"],["dc.contributor.author","Bayram, Oezguer"],["dc.contributor.author","Sari, Fatih"],["dc.contributor.author","Braus, Gerhard H."],["dc.contributor.author","Irniger, Stefan"],["dc.date.accessioned","2018-11-07T08:41:34Z"],["dc.date.available","2018-11-07T08:41:34Z"],["dc.date.issued","2010"],["dc.description.abstract","Progression through mitosis requires the activity of cyclin-dependent kinases (CDKs) associated with regulatory cyclin subunits. In the yeast Saccharomyces cerevisiae, Clb2 has the most important role among the four mitotic cyclins, Clb1-4, manifested by data showing that simultaneous deletion of the CLB1, CLB3 and CLB4 genes has only minor effects on mitosis. Thus, Clb2 alone is sufficient for all essential CDK functions in mitosis, such as the assembly of bipolar spindles and spindle elongation. Here, we show that a modification of Clb2, by the C-terminal addition of a Myc12 epitope, causes the loss of one specific mitotic function of Clb2. Strains carrying CLB2-MYC12 are nonviable in the absence of the CLB3 and CLB4 genes, because the modified Clb2 version fails to promote assembly of the mitotic spindle. In contrast, Clb2-Myc12 has no apparent defects in late mitotic functions and, furthermore, induces the switch from polarized to isotropic growth with similar efficiency as the endogenous Clb2. Thus, the presence of the Myc12 epitope selectively inactivates Clb2's capacity to promote spindle formation. Clb2-Myc12 represents therefore the first version of Clb2 impaired in one specific mitotic function. We conclude that the major mitotic functions of this cyclin can be unequivocally dissected."],["dc.identifier.doi","10.4161/cc.9.13.12082"],["dc.identifier.isi","000281205400035"],["dc.identifier.pmid","20581451"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19497"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Taylor & Francis Inc"],["dc.relation.issn","1551-4005"],["dc.relation.issn","1538-4101"],["dc.title","Dissection of mitotic functions of the yeast cyclin Clb2"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]