Peripheral apoptosis and limited clonal deletion during physiologic murine B lymphocyte development.

Self-reactive and polyreactive B cells generated during B cell development are silenced by either apoptosis, clonal deletion, receptor editing or anergy to avoid autoimmunity. The specific contribution of apoptosis to normal B cell development and self-tolerance is incompletely understood. Here, we quantify self-reactivity, polyreactivity and apoptosis during physiologic B lymphocyte development.

A heritable iron memory enables decision-making in .

The importance of memory in bacterial decision-making is relatively unexplored. We show here that a prior experience of swarming is remembered when encounters a new surface, improving its future swarming efficiency. We conducted >10,000 single-cell swarm assays to discover that cells store memory in the form of cellular iron levels.

Iron Memory in .

The importance of memory in bacterial decision-making is relatively unexplored. We show here that a prior experience of swarming is remembered when encounters a new surface, improving its future swarming efficiency. We conducted >10,000 single-cell swarm assays to discover that cells store memory in the form of cellular iron levels.

Peripheral death by neglect and limited clonal deletion during physiologic B lymphocyte development.

Autoreactive B cells generated during B cell development are inactivated by clonal deletion, receptor editing or anergy. Up to 97% of immature B cells appear to die before completing maturation, but the anatomic sites and reasons underlying this massive cell loss are not fully understood. Here, we directly quantitated apoptosis and clonal deletion during physiologic B lymphocyte development using Rosa26 apoptosis indicator mice.

Efflux-linked accelerated evolution of antibiotic resistance at a population edge.

Efflux is a common mechanism of resistance to antibiotics. We show that efflux itself promotes accumulation of antibiotic-resistance mutations (ARMs). This phenomenon was initially discovered in a bacterial swarm where the linked phenotypes of high efflux and high mutation frequencies spatially segregated to the edge, driven there by motility.