Publications by authors named "Cesar Augusto Vargas Garcia"

Measurements of cell size dynamics have revealed phenomenological principles by which individual cells control their size across diverse organisms. One of the emerging paradigms of cell size homeostasis is the , where the cell cycle duration is established such that the cell size increase from birth to division is independent of the newborn cell size. We provide a mechanistic formulation of the considering that cell size follows any .

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Under ideal conditions, Escherichia coli cells divide after adding a fixed cell size, a strategy known as the adder. This concept applies to various microbes and is often explained as the division that occurs after a certain number of stages, associated with the accumulation of precursor proteins at a rate proportional to cell size. However, under poor media conditions, E.

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Understanding how population-size homeostasis emerges from stochastic individual cell behaviors remains a challenge in biology. The unicellular green alga Chlamydomonas reinhardtii (Chlamydomonas) proliferates using a multiple fission cell cycle, where a prolonged G1 phase is followed by n rounds of alternating division cycles (S/M) to produce 2 daughters. A "Commitment" sizer in mid-G1 phase ensures sufficient cell growth before completing the cell cycle.

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Fission yeast cells prevent mitotic entry until a threshold cell surface area is reached. The protein kinase Cdr2 contributes to this size control system by forming multiprotein nodes that inhibit Wee1 at the medial cell cortex. Cdr2 node anchoring at the cell cortex is not fully understood.

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Background: How small, fast-growing bacteria ensure tight cell-size distributions remains elusive. High-throughput measurement techniques have propelled efforts to build modeling tools that help to shed light on the relationships between cell size, growth and cycle progression. Most proposed models describe cell division as a discrete map between size at birth and size at division with stochastic fluctuations assumed.

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At the single-cell level, noise arises from multiple sources, such as inherent stochasticity of biomolecular processes, random partitioning of resources at division, and fluctuations in cellular growth rates. How these diverse noise mechanisms combine to drive variations in cell size within an isoclonal population is not well understood. Here, we investigate the contributions of different noise sources in well-known paradigms of cell-size control, such as adder (division occurs after adding a fixed size from birth), sizer (division occurs after reaching a size threshold), and timer (division occurs after a fixed time from birth).

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The sample frequency and volume of blood that can be drawn from a single patient is meticulously restricted under the human subject protection protocols established by an institutional review board (IRB). Consequently, the amount of samples that can be taken during a particular experiment is limited. In order to ensure an effective experiment design, considerations must be taken choosing when to take patient samples.

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Inside individual cells, stochastic expression drives random fluctuations in gene product copy numbers, which corrupts functioning of both natural and synthetic genetic circuits. Dynamic models of genetic circuits are formulated stochastically using the chemical master equation framework. Since obtaining probability distributions can be computationally expensive in these models, noise is typically investigated through lower-order statistical moments (mean, variance, correlation, skewness, etc.

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Background: The main objective of flux balance analysis (FBA) is to obtain quantitative predictions of metabolic fluxes of an organism, and it is necessary to use an appropriate objective function to guarantee a good estimation of those fluxes.

Methodology: In this study, the predictive performance of FBA was evaluated, using objective functions arising from the linear combination of different cellular objectives. This approach is most suitable for eukaryotic cells, owing to their multiplicity of cellular compartments.

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