Spontaneous growth arrest of transformed melanocytes (resulting in benign “moles”) does not result from cell-autonomous oncogene-induced senescence, but can be explained by collective mechanisms used in normal tissue size control.
A mechanistic basis is provided for the regulative ability of the mammalian embryo offering a long-sought explanation for coordinating cell behaviors at the population level ensuring robustness in developmental outcome.
The double-gene-knockout pig is a valuable model to help understand the mechanisms of CD163 and pAPN in the infection of multiple viruses and offers excellent breeding materials for disease-resistant pigs.
Genetic and molecular analyses show that FOXC1 and FOXC2 play a role in controlling lymphatic valve maintenance as key mediators of mechanotransduction to control cytoskeletal organization and RhoA/ROCK signaling.
Relying on RNA fragments derived from degradation or partial template copying, non-enzymatic primer extension with strand displacement offers a novel and prebiotically plausible approach to RNA self-replication.