<i>LTE1</i> promotes exit from mitosis by multiple mechanisms

Falk, Jill; Campbell, Ian W; Joyce, Kelsey; Whalen, Jenna; Seshan, Anupama; Amon, Angelika

doi:10.1091/mbc.e16-08-0563

Cited by 23 publications

(41 citation statements)

References 58 publications

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“…We next asked whether the genes required for SPOC deficiency of swr1Δ cells were also required for SPOC deficiency of kin4Δ cells. In concordance with previous publications [26, 28], deletion of FEAR network components SPO12 and SLK19 rescued SPOC deficiency of kin4Δ cells. On the other hand, deletion of PRE9 , SLT2, SGF73 and SIC1 did not significantly impact upon SPOC deficiency of kin4Δ cells, albeit a slight reduction due to SIC1 and SGF73 deletion.…”

Section: Resultssupporting

confidence: 92%

“…The FEAR pathway ( SPO12 and SLK19 being FEAR components), on the other hand, is crucial for priming mitotic exit at several levels, such as at the level of Bfa1-Bub2 inactivation and, Cdc15 and Dbf2/Mob1 localization at SPBs [17, 18, 26]. Importantly, deletion of SPO12 or SLK19 reverted the SPOC deficiency of swr1Δ cells as well as kin4Δ cells [26, 28], highlighting the role of FEAR pathway in bypassing the immediate SPOC response. Unlike the FEAR pathway, the impairment of the proteasome and deletion of the mitotic CKI reverted the SPOC deficiency in swr1Δ but not kin4Δ cells.…”

Section: Discussionmentioning

confidence: 99%

“…Loss of microtubule-cortex interactions promotes Kin4 activity upon Bfa1. However, this is likely not the only factor that contributes to SPOC [26, 28, 29]. The compartmentalization of mitotic exit-activating and -inhibiting factors in daughter and mother cells respectively, was also shown to coordinate mitotic exit with the delivery of a nucleus into the daughter cell body [26, 30].…”

Section: Introductionmentioning

confidence: 99%

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SWR1 Chromatin Remodeling Complex Prevents Mitotic Slippage during Spindle Position Checkpoint Arrest

Caydasi

Khmelinskii

Darieva

et al. 2019

Preprint

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Faithful chromosome segregation in budding yeast requires correct positioning of the mitotic spindle along the mother to daughter cell polarity axis. When the anaphase spindle is not correctly positioned, a surveillance mechanism, named as the spindle position checkpoint (SPOC), prevents the progression out of mitosis until correct spindle positioning is achieved. How SPOC works on a molecular level is not wellunderstood. Here, we performed a genome-wide genetic screen to search for components required for SPOC. We identified the SWR1 chromatin-remodeling complex (SWR1-C) among the several novel factors that are essential for SPOC integrity. Cells lacking SWR1-C were able to activate SPOC upon spindle misorientation but underwent mitotic slippage upon prolonged SPOC arrest. This mitotic slippage required the Cdc14-early anaphase release pathway and other factors including the SAGA histone acetyltransferase complex, proteasome components, the mitotic cyclin-dependent kinase inhibitor Sic1 and the mitogen-activated protein kinase Slt2/Mpk1. Together, our data establish a novel link between chromatin remodeling and robust checkpoint arrest in late anaphase.

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Section: Resultssupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

SWR1 Chromatin Remodeling Complex Prevents Mitotic Slippage during Spindle Position Checkpoint Arrest

Caydasi

Khmelinskii

Darieva

et al. 2019

Preprint

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“…In S. cerevisiae , Lte1 is an activator of the MEN that localizes to the bud cortex 35 , 36 . This asymmetric distribution of Lte1 is maintained by the septin ring, which acts as a diffusion barrier between the mother and the bud 11 , 13 .…”

Section: Resultsmentioning

confidence: 99%

The anillin-related Int1 protein and the Sep7 septin collaborate to maintain cellular ploidy in Candida albicans

Orellana-Muñoz

Dueñas-Santero

Arnáiz‐Pita

et al. 2018

Sci Rep

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Variation in cell ploidy is a common feature of Candida albicans clinical isolates that are resistant to the antifungal drug fluconazole. Here, we report that the anillin-related protein Int1 interacts with septins for coupling cytokinesis with nuclear segregation. Loss of Int1 results in a rapid disassembly of duplicated septin rings from the bud neck at the onset of actomyosin ring contraction. Strikingly, this has no major impact on cytokinesis and septum formation. However, Int1 genetically interacts with the Sep7 septin, maintaining the diffusion barrier at the bud neck and guarantying a faithful nuclear segregation. Indeed, int1ΔΔ sep7ΔΔ mutant cells, in contrast to int1ΔΔ cdc10ΔΔ, undergo a premature activation of mitotic exit prior to the alignment of the mitotic spindle with the division axis, producing large multinucleated cells. Some of these multinucleated cells arise from trimeras similar to those observed upon fluconazole exposure. Finally, the defects in nuclear segregation could be in part due to the inability to maintain the Lte1 mitotic exit activator at the cortex of the daughter cell. These results suggest that Int1 and Sep7 play a role in maintaining genome stability by acting as a diffusion barrier for Lte1.

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“…Guanine nucleotide exchange factor LTE1 (LTE1) is a GDP-GTP exchange factor for GTP-binding protein involved in the termination of M phase and functions in the mitotic exit network. LTE1 as a signal promotes exiting from mitosis by multiple mechanisms [77]. Structural maintenance of chromosomes protein 4 (SMC4) is a central component of the condensin complex required for conversion of interphase chromatin into mitotic-like condense chromosomes [78].…”

Section: Cell Cycle and Multiplicationmentioning

confidence: 99%

Cuminal Inhibits Trichothecium roseum Growth by Triggering Cell Starvation: Transcriptome and Proteome Analysis

Zhang

et al. 2020

Microorganisms

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Trichothecium roseum is a harmful postharvest fungus causing serious damage, together with the secretion of insidious mycotoxins, on apples, melons, and other important fruits. Cuminal, a predominant component of Cuminum cyminum essential oil has proven to successfully inhibit the growth of T. roseum in vitro and in vivo. Electron microscopic observations revealed cuminal exposure impaired the fungal morphology and ultrastructure, particularly the plasmalemma. Transcriptome and proteome analysis was used to investigate the responses of T. roseum to exposure of cuminal. In total, 2825 differentially expressed transcripts (1516 up and 1309 down) and 225 differentially expressed proteins (90 up and 135 down) were determined. Overall, notable parts of these differentially expressed genes functionally belong to subcellular localities of the membrane system and cytosol, along with ribosomes, mitochondria and peroxisomes. According to the localization analysis and the biological annotation of these genes, carbohydrate and lipids metabolism, redox homeostasis, and asexual reproduction were among the most enriched gene ontology (GO) terms. Biological pathway enrichment analysis showed that lipids and amino acid degradation, ATP-binding cassette transporters, membrane reconstitution, mRNA surveillance pathway and peroxisome were elevated, whereas secondary metabolite biosynthesis, cell cycle, and glycolysis/gluconeogenesis were down regulated. Further integrated omics analysis showed that cuminal exposure first impaired the polarity of the cytoplasmic membrane and then triggered the reconstitution and dysfunction of fungal plasmalemma, resulting in handicapped nutrient procurement of the cells. Consequently, fungal cells showed starvation stress with limited carbohydrate metabolism, resulting a metabolic shift to catabolism of the cell's own components in response to the stress. Additionally, these predicaments brought about oxidative stress, which, in collaboration with the starvation, damaged certain critical organelles such as mitochondria. Such degeneration, accompanied by energy deficiency, suppressed the biosynthesis of essential proteins and inhibited fungal growth.fungicides to be used for postharvest treatment, reduced efficacy due to the emergence of pathogen resistance to these chemicals, and the growing public concerns over chemical residues in food and the environment have necessitated the seeking of alternative solutions to control the fungal spoilage and to guarantee food safety and consumer health [8].Essential oils (EOs), generally recognized as safe by the US Food and Drug Administration [9], are natural substances with established antimicrobial activities [10,11] and are a candidate instrument for controlling postharvest disease [12,13]. Nonetheless, this candidacy is compromised by the expensiveness of these natural substances due to their generally low yields. However, exploring their mode of actions is valuable to the development of novel alternatives.The multicomponent EOs attribute their mode of act...

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LTE1 promotes exit from mitosis by multiple mechanisms

Abstract: In budding yeast, the spindle position checkpoint ensures that cells exit from mitosis only when their spindle is properly aligned along the mother–bud axis. Exit from mitosis is controlled by both negative signals in the mother cell compartment and positive signals in the bud.

Cited by 23 publications

References 58 publications

SWR1 Chromatin Remodeling Complex Prevents Mitotic Slippage during Spindle Position Checkpoint Arrest

SWR1 Chromatin Remodeling Complex Prevents Mitotic Slippage during Spindle Position Checkpoint Arrest

The anillin-related Int1 protein and the Sep7 septin collaborate to maintain cellular ploidy in Candida albicans

Cuminal Inhibits Trichothecium roseum Growth by Triggering Cell Starvation: Transcriptome and Proteome Analysis

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