Snf5 and Swi3 subcomplex formation is required for SWI/SNF complex function in yeast

Zhou, Hao; Chen, Guidong; Dong, Chunming; Zhao, Xiaozhou; Shen, Zhongtian; Chen, Feilong; Liu, Beibei; Long, Jiafu

doi:10.1016/j.bbrc.2020.03.169

Cited by 4 publications

(3 citation statements)

References 36 publications

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“…(D) Ratio of relative growth between 4 and 0.1 mg/L uracil from (C) was plotted for all candidates was transcription, including three prefoldin subunit annotations (Figure 5A and Table S3). Physically interacting transcription factors were identified (Figure S3), such as members of the Complex Proteins Associated with Set1 (COMPASS) complex, Swd1, Swd3 and Sdc1 45 alongside the Swi3/Snf5 pair 46 among others that gave significant defects in low uracil (Figure 5B). We reasoned transcriptional regulators could be indirectly involved in Fur4 membrane trafficking, controlling gene expression of either essential genes not tested in the primary screen or mutants identified from the screen itself.…”

Section: Screen Enriched For Trafficking and Transcriptional Machinerymentioning

confidence: 99%

Fur4‐mediated uracil‐scavenging to screen for surface protein regulators

Paine

Ecclestone

MacDonald

2021

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Cell surface membrane proteins perform diverse and critical functions and are spatially and temporally regulated by membrane trafficking pathways. Although perturbations in these pathways underlie many pathologies, our understanding of these pathways at a mechanistic level remains incomplete. Using yeast as a model, we have developed an assay that reports on the surface activity of the uracil permease Fur4 in uracil auxotroph strains grown in the presence of limited uracil. This assay was used to screen a library of haploid deletion strains and identified mutants with both diminished and enhanced comparative growth in restricted uracil media. Factors identified, including various multisubunit complexes, were enriched for membrane trafficking and transcriptional functions, in addition to various uncharacterized genes. Bioinformatic analysis of expression profiles from many strains lacking transcription factors required for efficient uracil-scavenging validated particular hits from the screen, in addition to implicating essential genes not tested in the screen. Finally, we performed a secondary mating factor secretion screen to functionally categorize factors implicated in uracil-scavenging.

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Section: Screen Enriched For Trafficking and Transcriptional Machinerymentioning

confidence: 99%

Fur4‐mediated uracil‐scavenging to screen for surface protein regulators

Paine

Ecclestone

MacDonald

2021

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“…The other biological process significantly enriched was transcription, including 3 prefoldin subunits annotations (Figure 5A, Table S3). Physically interacting transcription factors were identified (Figure S2), such as members of the COMPASS complex, Swd1, Swd3, and Sdc1 44 alongside the Swi3/Snf5 pair 45 amongst others, all of which exhibit significant defects in low uracil (Figure 5B). We reasoned transcriptional regulators could be indirectly involved in Fur4 membrane trafficking, controlling gene expression of either essential genes not tested in the primary screen or mutants identified from the screen itself.…”

Section: Screen Enriched For Trafficking and Transcriptional Machinerymentioning

confidence: 99%

Fur4 mediated uracil-scavenging to screen for surface protein regulators

Paine

Ecclestone

MacDonald

2021

Preprint

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Cell surface membrane proteins perform diverse and critical functions and are spatially and temporally regulated by membrane trafficking pathways. Although perturbations in these pathways underlie many pathologies, our understanding of these pathways at a mechanistic level remains incomplete. Using yeast as a model, we have developed an assay that reports on the surface activity of the Fur4 uracil permease in uracil auxotroph strains grown in the presence of limited uracil. This assay was used to screen a haploid deletion library that identified mutants with both diminished and enhanced comparative growth in restricted uracil media. Factors identified, including various multi-subunit complexes, were enriched for membrane trafficking and transcriptional functions, in addition to various uncharacterised genes. Bioinformatic analysis of expression profiles from many strains lacking identified transcription factors required for efficient uracil-scavenging revealed they control expression of other uracil-scavenging factors, in addition to membrane trafficking genes essential for viability, and therefore not represented in the screen. Finally, we performed a secondary mating factor secretion screen to functionally categorise factors implicated in uracil-scavenging, most of which are conserved throughout evolution.

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“…The SWI/SNF (switching defective/sucrose non-fermenting) complex is a conserved ATP-dependent chromatin remodeling complex, which plays essential roles in coordinating chromatin architecture and gene expression among eukaryotes [ 1 ]. The SWI/SNF complex usually contains over 13 subunits, in which Snf5 as the core one is essential to the execution of nucleosome remodeling [ 1 , 2 , 3 , 4 , 5 ]. Snf5 is localized in the nucleus and can be re-located into the cytosol under hypoxic conditions [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

MoSnf5 Regulates Fungal Virulence, Growth, and Conidiation in Magnaporthe oryzae

Zhao

et al. 2022

JoF

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Snf5 (sucrose nonfermenting) is a core component of the SWI/SNF complexes and regulates diverse cellular processes in model eukaryotes. In plant pathogenic fungi, its biological function and underlying mechanisms remain unexplored. In this study, we investigated the biological roles of MoSnf5 in plant infection and fungal development in the rice blast pathogen Magnaporthe oryzae. The gene deletion mutants of MoSNF5 exhibited slower vegetative hyphal growth, severe defects in conidiogenesis, and impaired virulence and galactose utilization capacities. Domain dissection assays showed that the Snf5 domain and the N- and C-termini of MoSnf5 were all required for its full functions. Co-immunoprecipitation and yeast two-hybrid assays showed that MoSnf5 physically interacts with four proteins, including a transcription initiation factor MoTaf14. Interestingly, the ∆MoTaf14 mutants showed similar phenotypes as the ∆Mosnf5 mutants on fungal virulence and development. Moreover, assays on GFP-MoAtg8 expression and localization showed that both the ∆Mosnf5 and ∆MoTaf14 mutants were defective in autophagy. Taken together, MoSnf5 regulates fungal virulence, growth, and conidiation, possibly through regulating galactose utilization and autophagy in M. oryzae.

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Snf5 and Swi3 subcomplex formation is required for SWI/SNF complex function in yeast

Cited by 4 publications

References 36 publications

Fur4‐mediated uracil‐scavenging to screen for surface protein regulators

Fur4‐mediated uracil‐scavenging to screen for surface protein regulators

Fur4 mediated uracil-scavenging to screen for surface protein regulators

MoSnf5 Regulates Fungal Virulence, Growth, and Conidiation in Magnaporthe oryzae

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