The SWI/SNF chromatin remodeling complex: a critical regulator of metabolism.

The close relationship between chromatin and metabolism has been well-studied in recent years. Many metabolites have been found to be cofactors used to modify chromatin, and these modifications can in turn affect gene transcription. One chromatin-associated factor responsible for regulating transcription is the SWI/SNF complex, an ATP-dependent chromatin remodeler conserved throughout eukaryotes.

The E3 ubiquitin ligase SPOP controls resolution of systemic inflammation by triggering MYD88 degradation.

The response to systemic infection and injury requires the rapid adaptation of hematopoietic stem cells (HSCs), which proliferate and divert their differentiation toward the myeloid lineage. Significant interest has emerged in understanding the signals that trigger the emergency hematopoietic program. However, the mechanisms that halt this response of HSCs, which is critical to restore homeostasis, remain unknown.

PTPN14 regulates Roquin2 stability by tyrosine dephosphorylation.

Protein phosphorylation regulates a variety of cellular signaling pathways and fundamental mechanisms in cells. In this paper, we demonstrate that the mRNA decay factor Roquin2 is phosphorylated at tyrosine residue in position 691 in vivo. This phosphorylation disrupts the interaction with KLHL6, the E3 ligase for Roquin2.

Loss of KLHL6 promotes diffuse large B-cell lymphoma growth and survival by stabilizing the mRNA decay factor roquin2.

Kelch-like protein 6 (KLHL6) is an uncharacterized gene mutated in diffuse large B-cell lymphoma (DLBCL). Here we report that KLHL6 assembles with cullin3 to form a functional cullin-RING ubiquitin ligase. Mutations in KLHL6 inhibit its ligase activity by disrupting the interaction with cullin3.

Degradation of Cep68 and PCNT cleavage mediate Cep215 removal from the PCM to allow centriole separation, disengagement and licensing.

An intercentrosomal linker keeps a cell's two centrosomes joined together until it is dissolved at the onset of mitosis. A second connection keeps daughter centrioles engaged to their mothers until they lose their orthogonal arrangement at the end of mitosis. Centriole disengagement is required to license centrioles for duplication.

Restricting self-renewal signals within the stem cell niche: multiple levels of control.

Germline stem cells (GSCs) were the first stem cells demonstrated to be regulated by the microenvironment or niche in the Drosophila ovary a decade ago. In the Drosophila ovary, as a stem cell divides, one daughter remaining in the niche continues to self-renew, and the other daughter positioned outside the niche undergoes differentiation. The niche produces bone morphogenetic proteins (BMPs) that only act within one cell diameter to ensure that at every division only one of two GSC daughters self-renews and thus maintains a stable GSC pool.

New dimensions of the virus world discovered through metagenomics.

Metagenomic analysis of viruses suggests novel patterns of evolution, changes the existing ideas of the composition of the virus world and reveals novel groups of viruses and virus-like agents. The gene composition of the marine DNA virome is dramatically different from that of known bacteriophages. The virome is dominated by rare genes, many of which might be contained within virus-like entities such as gene transfer agents.

Neural crest cell plasticity. size matters.

Patterning and morphogenesis of neural crest-derived tissues within a developing vertebrate embryo rely on a complex balance between signals acquired by neural crest cells in the neuroepithelium during their formation and signals from the tissues that the neural crest cells contact during their migration. Axial identity of hindbrain neural crest is controlled by a combinatorial pattern of Hox gene expression. Cellular interactions that pattern neural crest involve signals from the same key molecular families that regulate other aspects of patterning and morphogenesis within a developing embryo, namely the BMP, SHH and FGF pathways.