SP140 represses specific loci by recruiting polycomb repressive complex 2 and NuRD complex.

SP140, a lymphocytic-restricted protein, is an epigenetic reader working as a corepressor of genes implicated in inflammation and orchestrating macrophage transcriptional programs to maintain cellular identity. Reduced SP140 expression is associated both to autoimmune diseases and blood cancers. However, the molecular mechanisms that link SP140 altered protein levels to detrimental effects on the immune response and cellular growth, as well as the interactors through which SP140 promotes gene silencing, remain elusive.

Iron starvation results in up-regulation of a probable siderophore transporter.

The response of the haloarchaeal model organism to iron starvation was analyzed at the proteome level by data-independent acquisition mass spectrometry. Cells grown in minimal medium with normal iron levels were compared to those grown under low iron conditions, with samples being separated into membrane and cytoplasmic fractions in order to focus on import/export processes which are frequently associated with metal homeostasis. Iron starvation not only caused a severe retardation of growth but also altered the levels of many proteins.

Biomolecular Condensates in Myeloid Leukemia: What Do They Tell Us?

Recent studies have suggested that several oncogenic and tumor-suppressive proteins carry out their functions in the context of specific membrane-less cellular compartments. As these compartments, generally referred to as onco-condensates, are specific to tumor cells and are tightly linked to disease development, the mechanisms of their formation and maintenance have been intensively studied. Here we review the proposed leukemogenic and tumor-suppressive activities of nuclear biomolecular condensates in acute myeloid leukemia (AML).

The NFIA-ETO2 fusion blocks erythroid maturation and induces pure erythroid leukemia in cooperation with mutant TP53.

The NFIA-ETO2 fusion is the product of a t(1;16)(p31;q24) chromosomal translocation, so far, exclusively found in pediatric patients with pure erythroid leukemia (PEL). To address the role for the pathogenesis of the disease, we facilitated the expression of the NFIA-ETO2 fusion in murine erythroblasts (EBs). We observed that NFIA-ETO2 significantly increased proliferation and impaired erythroid differentiation of murine erythroleukemia cells and of primary fetal liver-derived EBs.