Nuclear organization articles from across Nature Portfolio

Magda Bienko highlights a landmark paper by Lieberman-Aiden et al., which in 2009 reported the development of high-throughput chromosome conformation capture (Hi-C), revolutionizing the field of 3D genome biology.

A new study shows that age-dependent nuclear remodelling in cardiomyocytes (via age-related loss of nuclear lamins) contributes to cardiac dysfunction through a process that is conserved in flies, mice and nonhuman primates.

Under conditions of stress, autophagic degradation of nuclear and nucleolar components was found to promot.e youthfulness and delay aging by preserving nuclear architecture and preventing nucleolar expansion, in somatic cells. We also found that nuclear-material autophagy serves as an essential quality-control mechanism that contributes to sustaining germline immortally.

We found that aging is accompanied by a reduction in cardiomyocyte nuclear size and increased stiffness, dependent on loss of A-type lamins. Mechanistically, age-dependent nuclear remodeling represses expression of cardiogenic transcription factors that are required for heart contractility. Preserving lamin or transcription factors delays cardiac decline.

Nuclear actin polymerization helps facilitate chromosome compartment switches that can shift damaged DNA toward a nuclear environment that is favorable for DNA repair. Yet shifting multiple broken DNA strands together can also increase the likelihood of misjoining of the DNA ends and subsequent formation of translocations.

Aging is associated with an accumulation of myeloid-biased hematopoietic stem cells with reduced regenerative potential, but the underlying mechanisms remain unclear. A study by Wendorff et al. demonstrates that inactivation of a single epigenetic regulator — the plant homeodomain factor 6 (PHF6) — transcriptionally and functionally rejuvenates mouse aged hematopoietic stem cells.