Biology subjects

Schreck, C.

Publications and source records attributed to Schreck, C..

3 recordsLinked to original sources

bioRxiv2021

Bacterial filamentation drives colony chirality

Chirality is ubiquitous in nature, with consequences at the cellular and tissue scales. As Escherichia coli colonies expand radially, an orthogonal component of growth creates a pinwheel-like pattern that can be revealed by fluorescent markers. To elucidate the mechanistic basis of this colony chirality, we investigated its link to left-handed, single-cell twisting during E. coli elongation. While chemical and genetic manipulation of cell width altered single-cell twisting handedness, colonies ceased to be chiral rather than switching handedness, and anaerobic growth altered colony chirality without affecting single-cell twisting. Chiral angle increased with increasing temperature even when growth rate decreased. Unifying these findings, we discovered that colony chirality was associated with the propensity for cell filamentation. Inhibition of cell division accentuated chirality under aerobic growth and generated chirality under anaerobic growth. Thus, regulation of cell division is intrinsically coupled to colony chirality, providing a mechanism for tuning macroscale spatial patterning.

microbiology↗

bioRxiv2020

Cathepsin K is required for maintenance and regeneration of lymphopoiesis in vivo

In this study, we investigated the influence of the loss of Cathepsin K (Ctsk) gene on the hematopoietic system in vitro and in vivo. We found that cultures with Lineage- SCA1+ KIT+ (LSK) cells on Ctsk deficient stromal cells display reduced colony formation and proliferation, with increased differentiation, giving rise to repopulating cells with reduced ability to repopulate the donor LSK and T cell compartments in the bone marrow. Subsequent in vivo experiments showed impairment of lymphocyte numbers, but, gross effects on early hematopoiesis or myelopoiesis were not found. Most consistently in in vivo experimental settings, we found a significant reduction of (donor) T cell numbers in the bone marrow. Lymphocyte deregulation is also found in transplantation experiments, which revealed that Ctsk is required for optimal regeneration not only of T cells, but also of B cells. Interestingly, cell non-autonomous Ctsk regulates both B- and T cell numbers, but T cell numbers in the bone marrow require an additional autonomous Ctsk-dependent process. Thus, we show that Ctsk is required for the maintenance of hematopoietic stem cells in vitro, but in vivo, Ctsk deficiency most strongly affects lymphocyte homeostasis, particularly of T cells in the bone marrow.

cell biology↗

bioRxiv2018

Collective motion conceals fitness differences in crowded cellular populations

Many cellular populations are tightly-packed, for example microbial colonies and biofilms [39, 10, 41], or tissues and tumors in multi-cellular organisms [11, 29]. Movement of one cell inside such crowded assemblages requires movement of others, so that cell displacements are correlated over many cell diameters [28, 6, 31]. Whenever movement is important for survival or growth [15, 34, 38, 9], such correlated rearrangements could couple the evolutionary fate of different lineages. Yet, little is known about the interplay between mechanical stresses and evolution in dense cellular populations. Here, by tracking deleterious mutations at the expanding edge of yeast colonies, we show that crowding-induced collective motion prevents costly mutations from being weeded out rapidly. Joint pushing by neighboring cells generates correlated movements that suppress the differential displacements required for selection to act. Such mechanical screening of fitness differences allows the mutants to leave more descendants than expected under non-mechanical models, thereby increasing their chance for evolutionary rescue [2, 5]. Our work suggests that mechanical interactions generally influence evolutionary outcomes in crowded cellular populations, which has to be considered when modeling drug resistance or cancer evolution [1, 22, 34, 30, 36, 42].

biophysics↗