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Biology subjects

Maes, C.

Publications and source records attributed to Maes, C..

2 recordsLinked to original sources

The Sun within: active processes from two-temperature models

We propose an embedding of standard active particle models in terms of two-temperature processes. One temperature refers to an ambient thermal bath, and the other temperature effectively describes "hot spots," i.e., systems with few degrees of freedom showing important population homogenization or even inversion of energy levels as a result of activation. As a result, the effective Carnot efficiency would get much higher than for our standard macroscopic thermal engines, making connection with the recent conundrum of hot mitochondria. Moreover, that setup allows to quantitatively specify the resulting nonequilibrium driving, useful in particular for bringing the notion of heat into play, and making easy contact with thermodynamic features. Finally, we observe that the shape transition in the steady low-temperature behavior of run-and-tumble particles (with the interesting emergence of edge states at high persistence) is stable and occurs for all temperature differences, including close-to-equilibrium.

biophysics↗

Myeloid-biased HSC require Semaphorin 4A from the bone marrow niche for self-renewal under stress and life-long persistence

Tissue stem cells are hierarchically organized. Those that are most primitive serve as key drivers of regenerative response but the signals that selectively preserve their functional integrity are largely unknown. Here, we identify a secreted factor, Semaphorin 4A (Sema4A), as a specific regulator of myeloid-biased hematopoietic stem cells (myHSC), which are positioned at the top of the HSC hierarchy. Lack of Sema4A leads to exaggerated myHSC (but not downstream "balanced" HSC) proliferation after acute inflammatory stress, indicating that Sema4A enforces myHSC quiescence. Strikingly, aged Sema4A knock-out myHSC expand but almost completely lose reconstitution capacity. The effect of Sema4A is non cell-autonomous, since upon transplantation into Sema4A-deficient environment, wild-type myHSC excessively proliferate but fail to engraft long-term. Sema4A constrains inflammatory signaling in myHSC and acts via a surface receptor Plexin-D1. Our data support a model whereby the most primitive tissue stem cells critically rely on a dedicated signal from the niche for self-renewal and life-long persistence.

cell biology↗