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Genome-wide transcriptomic analysis of Arabdiopsis mutants controling nuclear size in comparison to the wildtype

ABSTRACT: Genome-wide transcriptomic analysis of Arabdiopsis mutants controling nuclear size in comparison to the wildtype

PROVIDER: PRJNA417457 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6264970_1.fastq.gz	Fastqsanger.gz
	SRR6264970_2.fastq.gz	Fastqsanger.gz
	SRR6264971_1.fastq.gz	Fastqsanger.gz
	SRR6264971_2.fastq.gz	Fastqsanger.gz
	SRR6264972_1.fastq.gz	Fastqsanger.gz

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Genome-wide transcriptomic analysis of Arabdiopsis mutants controling nuclear size in comparison to the wildtype

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Project description:How cells control the overall size of membrane-bound organelles is an important unanswered question of cell biology. Fission yeast cells maintain a nuclear size that is proportional to cellular size, resulting in a constant ratio between the nuclear and cellular volumes (N/C ratio). To shed light on nuclear size control we conducted a genome-wide visual screen of a fission yeast gene deletion collection for mutants altered in their N/C ratio, and found that defects in both nucleocytoplasmic mRNA transport and nuclear membrane proliferation alter the N/C ratio. Perturbing nuclear mRNA export causes general bulk accumulation of both mRNA and protein, and a N/C ratio increase which is dependent on new membrane synthesis. Dysregulation of nuclear membrane growth also results in an enlarged N/C ratio, and additionally generates an aberrant nuclear shape. We propose that both properly regulated nucleocytoplasmic transport and nuclear membrane growth are central for controlling nuclear size.

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SUN1/2 Controls Macrophage Polarization via Modulating Nuclear Size and Stiffness

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Budding yeast size control by titration of nuclear sites

Project description:This model is decribed in the article: Dilution and titration of cell-cycle regulators may control cell size in budding yeast Frank S. Heldt, Reece Lunstone, John J. Tyson, Bela Novak PLoS Comput Biol, October 2018, 14(10), e1006548, doi: 10.1371/journal.pcbi.1006548 Abstract: The size of a cell sets the scale for all biochemical processes within it, thereby affecting cellular fitness and survival. Hence, cell size needs to be kept within certain limits and relatively constant over multiple generations. However, how cells measure their size and use this information to regulate growth and division remains controversial. Here, we present two mechanistic mathematical models of the budding yeast (S. cerevisiae) cell cycle to investigate competing hypotheses on size control: inhibitor dilution and titration of nuclear sites. Our results suggest that an inhibitor-dilution mechanism, in which cell growth dilutes the transcriptional inhibitor Whi5 against the constant activator Cln3, can facilitate size homeostasis. This is achieved by utilising a positive feedback loop to establish a fixed size threshold for the START transition, which efficiently couples cell growth to cell cycle progression. Yet, we show that inhibitor dilution cannot reproduce the size of mutants that alter the cell’s overall ploidy and WHI5 gene copy number. By contrast, size control through titration of Cln3 against a constant number of genomic binding sites for the transcription factor SBF recapitulates both size homeostasis and the size of these mutant strains. Moreover, this model produces an imperfect ‘sizer’ behaviour in G1 and a ‘timer’ in S/G2/M, which combine to yield an ‘adder’ over the whole cell cycle; an observation recently made in experiments. Hence, our model connects these phenomenological data with the molecular details of the cell cycle, providing a systems-level perspective of budding yeast size control.

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