Jan Marcel Skotheim

The paper shows that dermal-epidermal junction geometry influences stem cell fate in mouse skin, with concave areas promoting proliferation and convex areas promoting differentiation.

The paper identifies regulators of nuclear-to-cell size ratio and shows nuclear size influences gene expression and cell fate.

This study expands the yeast genome with non-coding DNA and finds it reduces growth rate and endogenous mRNA concentration without affecting translation.

This study shows that non-coding DNA in yeast affects cell size and fitness by sequestering RNA polymerase, reducing transcript levels and impairing growth.

The paper shows that cell size affects mRNA concentrations, driving proteome changes through transcriptional regulation.

This study identifies FAM53C as a regulator of the G1/S cell cycle transition, showing it interacts with DYRK1A and affects cell cycle progression in cultured cells and organoids.

This study shows that yeast cells adapt to changes in mitochondrial DNA copy number through retrograde signaling and protein dosage compensation, allowing robust growth despite mtDNA fluctuations.

This study shows that phosphorylation stabilizes Rb by promoting its dissociation from chromatin, revealing a mechanism linking chromatin association to protein degradation.

The paper shows that cell size affects SBF and Whi5 chromatin binding to regulate the Start transition in budding yeast by altering their copy-number ratio and chromatin affinity.

This study shows that cell enlargement drives proteome remodeling and shortens replicative lifespan in yeast, independent of known aging factors.

This study shows that larger cells are more resistant to ferroptosis due to higher glutathione levels and lower lipid peroxides.

The paper identifies division asymmetry as the main driver of cell size variability in budding yeast, showing it outweighs G1/S size control effects.

This study shows that cell size autonomously regulates the G1/S transition in mammalian epidermal stem cells, independent of extracellular signals.

The paper confirms the Product neutrality function accurately predicts double mutant fitness in budding yeast and shows it emerges from mechanistic models of cell growth.

The paper develops human tri-lineage brain microtissues composed of neurons, astrocytes, and microglia, showing they recapitulate cell-cell interactions and pathological processes.

The paper shows that intracellular diffusion in fission yeast increases with cell size, linked to changes in proteome composition and DNA-to-cytoplasm ratio.

The paper shows genome concentration limits transcription and affects proteome composition in E. coli, with effects detectable in nutrient-rich conditions.

The paper shows that polyploidy in C. elegans intestine increases transcriptional output and supports biosynthesis by compensating for mRNA dilution through increased RNA Polymerase II loading.

The paper identifies RNAPII as the limiting factor for transcription scaling with cell size in budding yeast and shows that mRNA stability feedback compensates for sub-linear transcription growth.

The paper simulates the evolution of cell size control mechanisms and finds that adders or sizers emerge based on cell cycle structure and selective pressures.

This study shows that reducing genomic DNA content delays zygotic genome activation in Xenopus embryos, supporting the nuclear-to-cytoplasmic ratio model.

The paper challenges a model proposing that protein synthesis increases in pre-Start G1, finding that Whi5 concentration remains constant and Cln3 increase is not due to synthesis.

This paper introduces SMAC-seq, a method for long-range chromatin accessibility mapping in eukaryotes, and demonstrates its application in yeast.

This study develops a CRISPR/Cas9 method to reversibly disrupt specific transcription factor-DNA interactions and assess their functional impact on gene expression and cell division.

This paper introduces ChAR-seq, a method to map RNA-to-DNA contacts genome-wide, identifying chromatin-bound RNA targets such as nascent transcripts and trans-associated RNAs.