Fact 1. P16Ink4a causes senescence in aging cells
Hypothesis1a : p16ink4a causes senescence because aging cells are more frailty, have more DNA damage and more stress as a result of methylation changes a.k.a. epigenetic clock
Hypothesis 1b: p16ink4a causes senescence because itself is more upregulated as a result of age related hypomethylation
Hypotheis 1c: p16 ink4a causes senescence as it senses the epigenetic clock
Fact2 hTERT expression inhibits p16ink4a
also here
Hypothesis 2: this is a way for stem cells to avoid age related senescence
Fact3a in some epithelial cell cultures p16ink4a causes premature senescence, these cultures lack cell-cell adhesion
Fact3b in some epithelial telomere immortalized cells there is accelerated epigenetic aging
Hypothesis 3: lack of cell-cell adhesion accelerates epigenetic aging
Fact4: There is a growing body of evidence that suggests induction of epithelial cell migration is associated with upregulation of p16expression
Hypothesis 4a: epithelial cell migration accelerates epigenetic clock
Hypothesis 4b: gastrulation accelerates epigenetic clock
Hypothesis 4c: the epigenetic clock synchronizes cells in embryogenesis in triploblastic animals
Hypothesis 4d: the epigentic clock continues to tick after adult state is reached and results in epigenetic damage to the cells, causing cancer or mass senescence. Both fatal.
Fact5a: Diploblastic animals do not gastrulate
Fact5b: Diploblastic animals have all kinds of lifespans and sexual reproductive strategies
Fact5c: Triploblastic animals are more committed to strict lifespans and strict sexual reproduction
Hypothesis 5a: Gastrulation had enormous evolutionary advantages, see Cambrian explosion, but it also brought about strict lifespan regulation as a pleiotropic effect of more complex embryogenesis
Hypotheis 5b: Animals evolved "cheap hacks" to trick the epigenetic clock, for example Fact2
Hypothesis1a : p16ink4a causes senescence because aging cells are more frailty, have more DNA damage and more stress as a result of methylation changes a.k.a. epigenetic clock
Hypothesis 1b: p16ink4a causes senescence because itself is more upregulated as a result of age related hypomethylation
Hypotheis 1c: p16 ink4a causes senescence as it senses the epigenetic clock
Fact2 hTERT expression inhibits p16ink4a
also here
Hypothesis 2: this is a way for stem cells to avoid age related senescence
Fact3a in some epithelial cell cultures p16ink4a causes premature senescence, these cultures lack cell-cell adhesion
Fact3b in some epithelial telomere immortalized cells there is accelerated epigenetic aging
Hypothesis 3: lack of cell-cell adhesion accelerates epigenetic aging
Fact4: There is a growing body of evidence that suggests induction of epithelial cell migration is associated with upregulation of p16expression
Hypothesis 4a: epithelial cell migration accelerates epigenetic clock
Hypothesis 4b: gastrulation accelerates epigenetic clock
Hypothesis 4c: the epigenetic clock synchronizes cells in embryogenesis in triploblastic animals
Hypothesis 4d: the epigentic clock continues to tick after adult state is reached and results in epigenetic damage to the cells, causing cancer or mass senescence. Both fatal.
Fact5a: Diploblastic animals do not gastrulate
Fact5b: Diploblastic animals have all kinds of lifespans and sexual reproductive strategies
Fact5c: Triploblastic animals are more committed to strict lifespans and strict sexual reproduction
Hypothesis 5a: Gastrulation had enormous evolutionary advantages, see Cambrian explosion, but it also brought about strict lifespan regulation as a pleiotropic effect of more complex embryogenesis
Hypotheis 5b: Animals evolved "cheap hacks" to trick the epigenetic clock, for example Fact2
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