Reviews & Analysis

Unlike somatic cells, stem cells persist throughout life, which may increase their risk of accumulating DNA damage. recent studies indicate that stem cells use different mechanisms (such as the error-prone non-homologous end joining pathway) from somatic cells to maintain genomic integrity, which could have deleterious consequences for their long-term function.

The ability of growth factors and receptor Tyr kinases of the epidermal growth factor receptor (EGFR)/ERBB family to regulate cellular function is controlled by positive and negative feedback loops. These can decode ligand specificity, transform graded inputs into digital outputs and regulate response kinetics. Aberrant feedback can lead to pathologies, including cancer.

Dedifferentiation, transdifferentiation and reprogramming could all be exploited to replace lost cells and tissues. Studies are aiming to understand the molecular details of these processes and to elucidate the advantages of one process over another for use in regenerative medicine.

The MRE11 complex mediates repair of DNA double-strand breaks and is essential for genome stability. Structural studies and mouse models are increasing our understanding of how the different components of this complex together coordinate the damage response.

Mesenchymal stem cells (MSCs) are multipotent progenitors derived from tissue stroma that differentiate into adipocytes, chondrocytes and osteoblasts when expandedin vitro. Although the properties of the in vitro-expanded progeny are well defined, the in vivobiology of MSCs is only just beginning to be elucidated.

Single-cell measurements and lineage-tracing experiments are revealing that cell-to-cell variability is often the result of deterministic processes, despite the existence of intrinsic noise in molecular networks. As this determinism usually represents uncharacterized molecular regulatory mechanisms, cell-to-cell variability should be studied as a discipline of molecular cell biology.