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Transcriptional and chromatin-based partitioning mechanisms uncouple protein scaling from cell size

ABSTRACT: Transcriptional and chromatin-based partitioning mechanisms uncouple protein scaling from cell size

PROVIDER: PRJNA705222 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13799000_1.fastq.gz	Fastqsanger.gz
	SRR13799000_2.fastq.gz	Fastqsanger.gz
	SRR13799001_1.fastq.gz	Fastqsanger.gz
	SRR13799001_2.fastq.gz	Fastqsanger.gz
	SRR13799002_1.fastq.gz	Fastqsanger.gz

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Transcriptional and chromatin-based partitioning mechanisms uncouple protein scaling from cell size

Project description:Biosynthesis scales with cell size such that protein concentrations generally remain constant as cells grow. As an exception, synthesis of the cell-cycle inhibitor Whi5 ‘sub-scales’ with cell size so that its concentration is lower in larger cells to promote cell-cycle entry. Here, we find that a transcriptional control uncouples Whi5 synthesis from cell size and, screening for similar genes, identify histones as the major class of sub-scaling transcripts besides WHI5. Histone synthesis is thereby matched to genome content rather than cell size. Such sub-scaling proteins are challenged by asymmetric cell division because proteins are typically partitioned in proportion to new-born cell volume. To avoid this fate, Whi5 uses chromatin-binding to partition similar protein amounts to each new-born cell regardless of cell size. Finally, disrupting both Whi5 synthesis and chromatin-based partitioning compromises G1 size control. Thus, specific transcriptional and partitioning mechanisms determine protein sub-scaling to control cell size.

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Transcriptional and chromatin-based partitioning mechanisms uncouple protein scaling from cell size.

Project description:Biosynthesis scales with cell size such that protein concentrations generally remain constant as cells grow. As an exception, synthesis of the cell-cycle inhibitor Whi5 "sub-scales" with cell size so that its concentration is lower in larger cells to promote cell-cycle entry. Here, we find that transcriptional control uncouples Whi5 synthesis from cell size, and we identify histones as the major class of sub-scaling transcripts besides WHI5 by screening for similar genes. Histone synthesis is thereby matched to genome content rather than cell size. Such sub-scaling proteins are challenged by asymmetric cell division because proteins are typically partitioned in proportion to newborn cell volume. To avoid this fate, Whi5 uses chromatin-binding to partition similar protein amounts to each newborn cell regardless of cell size. Disrupting both Whi5 synthesis and chromatin-based partitioning weakens G1 size control. Thus, specific transcriptional and partitioning mechanisms determine protein sub-scaling to control cell size.

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Differential scaling of gene expression with cell size may explain size control in budding yeast.

Project description:Yeast cells must grow to a critical size before committing to division. It is unknown how size is measured. We find that as cells grow, mRNAs for some cell cycle activators scale faster than size, increasing in concentration, while mRNAs for some inhibitors scale slower than size, decreasing in concentration. Size-scaled gene expression could cause an increasing ratio of activators to inhibitors with size, triggering cell cycle entry. Consistent with this, expression of the CLN2 activator from the promoter of the WHI5 inhibitor, or vice versa, interfered with cell size homeostasis, yielding a broader distribution of cell sizes. We suggest that size homeostasis comes from differential scaling of gene expression with size. Such regulation of gene expression as a function of cell size could affect many cellular processes.

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Differential scaling of gene expression with cell size may explain size control in budding yeast.

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Differential scaling between G1 protein production and cell size dynamics promotes commitment to the cell division cycle in budding yeast

Project description:In the unicellular eukaryote Saccharomyces cerevisiae, Cln3–cyclin-dependent kinase activity enables Start, the irreversible commitment to the cell division cycle. However, the concentration of Cln3 has been paradoxically considered to remain constant during G1, due to the presumed scaling of its production rate with cell size dynamics. Measuring metabolic and biosynthetic activity during cell cycle progression in single cells, we found that cells exhibit pulses in their protein production rate. Rather than scaling with cell size dynamics, these pulses follow the intrinsic metabolic dynamics, peaking around Start. Using a viral- based bicistronic construct and targeted proteomics to measure Cln3 at the single-cell and population levels, we show that the differential scaling between protein production and cell size leads to a temporal increase in Cln3 concentration, and passage through Start. This differential scaling causes Start in both daughter and mother cells across growth conditions. Thus, uncou- pling between two fundamental physiological parameters drives cell cycle commitment.

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Differential scaling between G1 protein production and cell size dynamics promotes commitment to the cell division cycle in budding yeast

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Characterization of proteome-size scaling by integrative omics reveals mechanisms of proliferation control in cancer

Project description:Many cell types exhibit remarkable size homogeneity through successive divisions. In both yeast and humans, size homogeneity during division cycles is a result of tight control on the concentration of cell-cycle inhibitors such as WHI5 or RB1 (Retinoblastoma 1) proteins respectively. However, size control is often lost during oncogenesis, correlating with aggression. How size control is affected by mutations which drive proliferation, such as those of the RAS-ERK pathway, or even loss of RB1 itself, is poorly understood. Using quantitative single cell imaging of different melanoma cell lines, we show that melanoma cells exhibit both inter- and intra-line size variability. Integration of imaging with multi-omic data demonstrates that the translation machinery, G2 regulators, inflammatory mediators and growth-regulatory proteins are key determinants of size in melanoma. Theoretical modelling suggests that the cell size of daughter cells is determined by biosynthetic processes and engagement of stress responses in the mother. Biosynthesis and stress in mother cells impacts the synthesis of heritable prodivision factors like Cyclin D1 (CCND1) which control cell progression by inhibiting RB1 in concentration dependent fashions Small cell sizes and uniform populations are driven by robust DNA repair and increased levels of biosynthetic factors which promote CCDN1 accumulation. We propose that increased size and size-heterogeneity in BRAF and NRAS mutated cells is determined by stress or DNA damage in mother’s division cycle that slows cycle progression in the daughters. Such events lead to increased size and senescent-like states. Taken together our data suggest that oncogenic events, such as the dysregulation of MAPK signalling, provide a means to circumvent normal mechanisms of size regulation and increase cell-to-cell variations in size which may drive disease.

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