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Transcriptional profiling and localization of GUL-1, a COT-1 pathway component, in Neurospora crassa

•gul-1 affects transcript abundance of multiple genes in the COT-1 pathway.•Genes involved in cell wall remodelling and other processes are affected.•GUL-1 traffics as aggregates in a microtubule- dependent manner .•Stress resulted in a 2-3-fold increase of GUL-1 aggregate association with nuclei. I...

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Published in:Fungal genetics and biology 2019-05, Vol.126, p.1-11
Main Authors: Herold, Inbal, Kowbel, David, Delgado-Álvarez, Diego L., Garduño-Rosales, Marisela, Mouriño-Pérez, Rosa R., Yarden, Oded
Format: Article
Language:English
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Summary:•gul-1 affects transcript abundance of multiple genes in the COT-1 pathway.•Genes involved in cell wall remodelling and other processes are affected.•GUL-1 traffics as aggregates in a microtubule- dependent manner .•Stress resulted in a 2-3-fold increase of GUL-1 aggregate association with nuclei. Impairment of theNeurospora crassaCOT-1 kinase results in defects in hyphal polarity. Some of these effects are partially suppressed by inactivation of gul-1 (encoding an mRNA-binding protein involved in translational regulation). Here, we report on the transcriptional profiling of cot-1 inactivation and demonstrate that gul-1 affects transcript abundance of multiple genes in the COT-1 pathway, including processes such as cell wall remodeling, nitrogen and amino acid metabolism. The GUL-1 protein itself was found to be distributed within the entire hyphal cell, along with a clear presence of aggregates that traffic within the cytoplasm. Live imaging of GUL-1-GFP demonstrated that GUL-1 transport is microtubule-dependent. Cellular stress, as imposed by the presence of the cell wall biosynthesis inhibitor Nikkomycin Z or by nitrogen limitation, resulted in a 2–3-fold increase of GUL-1 aggregate association with nuclei. Taken together, this study demonstrates that GUL-1 affects multiple processes, its function is stress-related and linked with cellular traffic and nuclear association.
ISSN:1087-1845
1096-0937
DOI:10.1016/j.fgb.2019.01.010