Formation of Magnesium Carbonates on Earth and Implications for Mars.

Magnesium carbonates have been identified within the landing site of the Perseverance rover mission. This study reviews terrestrial analog environments and textural, mineral assemblage, isotopic, and elemental analyses that have been applied to establish formation conditions of magnesium carbonates. Magnesium carbonates form in five distinct settings: ultramafic rock-hosted veins, the matrix of carbonated peridotite, nodules in soil, alkaline lake, and playa deposits, and as diagenetic replacements within lime-and dolostones.

The histone H2A deubiquitinase Usp16 regulates hematopoiesis and hematopoietic stem cell function.

Epigenetic mechanisms play important regulatory roles in hematopoiesis and hematopoietic stem cell (HSC) function. Subunits of polycomb repressive complex 1 (PRC1), the major histone H2A ubiquitin ligase, are critical for both normal and pathological hematopoiesis; however, it is unclear which of the several counteracting H2A deubiquitinases functions along with PRC1 to control H2A ubiquitination (ubH2A) level and regulates hematopoiesis in vivo. Here we investigated the function of Usp16 in mouse hematopoiesis.

Allogeneic Th1 cells home to host bone marrow and spleen and mediate IFNγ-dependent aplasia.

Bone marrow graft failure and poor graft function are frequent complications after hematopoietic stem cell transplantation and result in significant morbidity and mortality. Both conditions are associated with graft-versus-host disease (GVHD), although the mechanism remains undefined. Here we show, in 2 distinct murine models of GVHD (complete MHC- and class II-disparate) that mimic human peripheral blood stem cell transplantation, that Th1 CD4(+) cells induce bone marrow failure in allogeneic recipients.

FLT3-ITD cooperates with inv(16) to promote progression to acute myeloid leukemia.

The inversion of chromosome 16 in the inv(16)(p13q22) is one of the most frequent cytogenetic abnormalities observed in acute myeloid leukemia (AML). The inv(16) fuses the core binding factor (CBF) beta subunit with the coiled-coil rod domain of smooth muscle myosin heavy chain (SMMHC). Expression of CBFbeta-SMMHC in mice does not promote AML in the absence of secondary mutations.

Expression of a non-DNA-binding isoform of Helios induces T-cell lymphoma in mice.

Helios is a zinc-finger protein belonging to the Ikaros family of transcriptional regulators. It is expressed, along with Ikaros, throughout early stages of thymocyte development where it quantitatively associates with Ikaros through C-terminal zinc-finger domains that mediate heterodimerization between Ikaros family members. To understand the role of Helios in T-cell development, we used a retroviral vector to express full-length Helios or a Helios isoform that lacked the N-terminal DNA-binding domain in hematopoietic progenitor cells of reconstituted mice.

The ETS family transcription factor PU.1 is necessary for the maintenance of fetal liver hematopoietic stem cells.

PU.1 is a member of the ETS family of transcription factors and is required for the development of multiple hematopoietic lineages. PU.

Activated Notch2 potentiates CD8 lineage maturation and promotes the selective development of B1 B cells.

Although studies have shown that the Notch2 family member is critical for embryonic development, little is known concerning its role in hematopoiesis. In this study, we show that the effects of an activated form of Notch2 (N2IC) on the T-cell lineage are dosage related. High-level expression of N2IC results in the development of T-cell leukemias.

Mutation of CpGs in the murine stem cell virus retroviral vector long terminal repeat represses silencing in embryonic stem cells.

Although DNA methylation and transcriptional repression are generally associated, a causal role for DNA methylation in silencing of retroviral vectors has not been established. The newer generation murine stem cell virus retroviral vector (MSCV) lacks many of the repressive cis-acting DNA sequences identified in Moloney murine leukemia virus but remains sensitive to transcriptional silencing in various cell types. To determine the contribution of cytosine methylation to MSCV silencing, we mutated CpG dinucleotides located in the MSCV long terminal repeat (LTR) that are clustered in the U3 region and directly spanning the transcription start site in the R region.

Mechanisms that regulate silencing of gene expression from retroviral vectors.

The propensity of retroviruses toward transcriptional silencing limits their value as gene therapy vectors. Silencing has been shown to be particularly robust when stem cells are used for transduction, posing a significant problem for gene therapy of hematologic diseases. Stability of proviral expression with newer generation vectors is significantly improved over that obtainable with original vectors based on Moloney murine leukemia virus (MoMLV).

Epidermal growth factor (EGF)-like repeats of human tenascin-C as ligands for EGF receptor.

Signaling through growth factor receptors controls such diverse cell functions as proliferation, migration, and differentiation. A critical question has been how the activation of these receptors is regulated. Most, if not all, of the known ligands for these receptors are soluble factors.

Human papillomavirus DNA replication compartments in a transient DNA replication system.

Many DNA viruses replicate their genomes at nuclear foci in infected cells. Using indirect immunofluorescence in combination with fluorescence in situ hybridization, we colocalized the human papillomavirus (HPV) replicating proteins E1 and E2 and the replicating origin-containing plasmid to nuclear foci in transiently transfected cells. The host replication protein A (RP-A) was also colocalized to these foci.

Association of the human papillomavirus type 11 E1 protein with histone H1.

The E1 and E2 proteins are the only virus-encoded factors required for human papillomavirus (HPV) DNA replication. The E1 protein is a DNA helicase responsible for initiation of DNA replication at the viral origin. Its recruitment to the origin is facilitated by binding to E2, for which specific recognition elements are located at the origin.