The different polymerases at eukaryotic replication forks achieve their asymmetric placement on the leading and lagging strands through exclusion processes that prevent their function on the 'wrong' strand.

When mismatch repair is compromised heterozygous loss of Pol ε proofreading is sufficient to drive a subset of the observed clinical characteristics of Pol ε tumors.

Shark's T cells suggest plasticity in diversification mechanisms used by vertebrate lymphocytes, including somatic hypermutation in the thymus.

The TPL corepressor binds to the core mediator complex through MED21 to inhibit transcription while simultaneously priming repressed genes for rapid reactivation.

The canonical model that the bacterial replisome tightly holds on to its polymerases is challenged by the visualization of rapid holoenzyme exchange, both in vitro and in vivo.

Translesion polymerase kappa promotes replication fork restart to maintain genome stability during conditions of nucleotide deprivation.

Quantitative binding and kinetic assays on DNA polymerases η and δ define the mechanism for polymerase exchange during human translesion DNA synthesis across a UV-induced lesion on the lagging strand.

Longitudinal neuroimaging models reveal that cross-sectional indices of brain age do not significantly relate to ongoing brain change, that is, brain aging, but to lifelong, stable variations in brain structure emerging in early life.

Pre-hematopoietic stem cells emerge from the aortic floor according to two radically different morphodynamics whose biomechanics rely on controlling apicobasal polarity in hemogenic precursors, which may impact on their fate.

RNA polymerase III plays a crucial role in controlling virulence in response to environmental changes and provides a new molecular perspective into the development of asymptomatic malaria.