Ever-evolving insights into the cellular and molecular drivers of lymphoid cell development.

Lymphocytes play a critical role in adaptive immunity and defense mechanisms, but the molecular mechanisms by which hematopoietic stem and progenitor cells differentiate into T and B lymphocytes are not fully established. Pioneer studies identify several transcription factors essential for lymphoid lineage determination. Yet, many questions remain unanswered about how these transcription factors interact with each other and with chromatin at different developmental stages.

A time- and single-cell-resolved model of murine bone marrow hematopoiesis.

The paradigmatic hematopoietic tree model is increasingly recognized to be limited, as it is based on heterogeneous populations largely defined by non-homeostatic assays testing cell fate potentials. Here, we combine persistent labeling with time-series single-cell RNA sequencing to build a real-time, quantitative model of in vivo tissue dynamics for murine bone marrow hematopoiesis. We couple cascading single-cell expression patterns with dynamic changes in differentiation and growth speeds.

Intravital Microscopy for Hematopoietic Studies.

The bone marrow (BM) is home to numerous cell types arising from hematopoietic stem cells (HSCs) and nonhematopoietic mesenchymal stem cells, as well as stromal cell components. Together they form the BM microenvironment or HSC niche. HSCs critically depend on signaling from these niches to function and survive in the long term.

mA RNA modifications: Key regulators of normal and malignant hematopoiesis.

Post-transcriptional RNA modifications determine RNA fate by influencing numerous processes such as translation, decay and localization. One of the most abundant RNA modifications is N-methyladenoside (mA), which has been shown to be important in healthy as well as malignant hematopoiesis. Several proteins representing key players in mA RNA biology, such as mA writers, erasers and readers, were recently reported to be essential for hematopoietic stem cell (HSC) function.

Metalloproteinase inhibition reduces AML growth, prevents stem cell loss, and improves chemotherapy effectiveness.

Acute myeloid leukemia (AML) is a blood cancer of the myeloid lineage. Its prognosis remains poor, highlighting the need for new therapeutic and precision medicine approaches. AML symptoms often include cytopenias linked to loss of healthy hematopoietic stem and progenitor cells (HSPCs).