Back to David's theory of evolution: planned cell death (Evolution)

by David Turell @, Friday, July 17, 2020, 05:32 (466 days ago) @ David Turell

Obviously programmed into the code of life:

"Chromatin instability and mitochondrial decline are conserved processes that contribute to cellular aging. Although both processes have been explored individually in the context of their distinct signaling pathways, the mechanism that determines which process dominates during aging of individual cells is unknown. We show that interactions between the chromatin silencing and mitochondrial pathways lead to an epigenetic landscape of yeast replicative aging with multiple equilibrium states that represent different types of terminal states of aging. The structure of the landscape drives single-cell differentiation toward one of these states during aging, whereby the fate is determined quite early and is insensitive to intracellular noise. Guided by a quantitative model of the aging landscape, we genetically engineered a long-lived equilibrium state characterized by an extended life span.


"Many damage factors, including chromatin instability, mitochondrial dysfunction, and reactive oxygen species (Display footnote number, contribute to cellular aging. In each individual cell, how these factors combine to drive the aging process remains unclear. For instance, aging could be driven by independent damage mechanisms that accumulate at varying rates, resulting in different aged phenotypes in individual cells, or, alternatively, by the deterioration of overall cellular condition, leading to a common aging pathway in all cells. Single-cell analysis can reveal which scenario actually underlies the aging process. We investigated replicative aging of the yeast Saccharomyces cerevisiae, a genetically tractable model for the aging of mitotic cell types such as stem cells (Display footnote number. Yeast aging research has focused on life span, as measured by the number of cell divisions before death

"Cellular aging can thus be considered a fatedecision process, in which single cells age toward either silencing loss and nucleolar decline or hemedepletion and mitochondrial decline. This process can be viewed as a divergent progression on a Sir2-HAP landscape, which can be reshaped by model-guided genetic perturbations, thereby enriching a long-lived mode of aging."

Comment: It is obvious cell death is planned by design, just whole organisms are planned for death. Part of God's design.

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