RT Journal Article SR Electronic T1 In Lyl1-/- mice, adipose stem cell vascular niche impairment leads to premature development of fat tissues JF bioRxiv FD Cold Spring Harbor Laboratory SP 2020.04.24.059683 DO 10.1101/2020.04.24.059683 A1 Abid Hussain A1 Leila El Kebriti A1 Virginie Deleuze A1 Yaël Glasson A1 Nelly Pirot A1 Danièle Mathieu A1 Valérie Pinet YR 2020 UL http://biorxiv.org/content/early/2020/04/25/2020.04.24.059683.abstract AB Lymphoblastic leukemia-derived sequence 1 (Lyl1) encodes a hematopoietic- and endothelial-specific transcriptional factor. Lyl1-deficient mice are viable, but they display mild hematopoietic and vascular defects. Here, we report that young Lyl1-/- mice exhibit transient obesity associated with general expansion of adipose tissues and unrelated to food intake. The increased fat tissue development in Lyl1-/- mice resulted from an earlier adipocyte differentiation of adipose stem cells (ASCs) through non-cell autonomous mechanisms. Specifically, we found that in Lyl1-/- mice, the vascular structures of adipose tissues are unstable, more prone to angiogenesis and, consequently, cannot maintain adipose progenitors in the niche vessel wall. Together, our data show that in Lyl1-/- mice, the impaired vascular compartment of the adipose niche promotes uncontrolled ASC activation and differentiation, leading to early adipocyte expansion and premature depletion of ASCs. Our study highlights the major structural role of the adipose tissue vascular niche in coordinating stem cell self-renewal and differentiation into adipocytes.Competing Interest StatementThe authors have declared no competing interest.