A comprehensive transcriptome and metabolome dataset for Erigeron breviscapus (Asteraceae) response to different light intensities - Nature

Submicron IR microscopy is opening new opportunities in biological sciences with the development of a new technique: optical photothermal infrared (O-PTIR) spectroscopy. Developments in life sciences research are playing an increasingly important role in global health, and advancements in technology have the potential to offer new and improved approaches to support the health and wellbeing of people worldwide.

The fusion of two cells is a decisive event in the sexual reproduction of many organisms. In fungi, cells must not only bring their membranes together and merge them, but also locally open their protective cell wall. A study conducted at the University of Geneva (UNIGE) shows how a mechanism that prevents cells from repairing their wall at the fusion site makes this process irreversible. Published in the journal Current Biology, these findings provide new insights into how cells coordinate fusion and repair mechanisms and could ultimately open new avenues for targeting the cell wall of pathogenic fungi. Unlike animal cells, fungal cells are surrounded by a rigid cell wall. This structure protects them and allows them to withstand the internal pressure exerted by their cellular contents. When two cells fuse, notably during sexual reproduction, this wall must be locally degraded to allow the membranes of the two cells to merge. Once this step has been completed, fusion normally proceeds until a single cell is formed.

We’re sharing this article early to provide faster access to peer-reviewed, accepted research. It is citable and carries a permanent DOI. This version is subject to further edits and will be replaced automatically by the final Version of Record. All legal disclaimers apply. AbstractFunctional recovery after spinal cord injury (SCI) remains challenging, requiring therapeutic targets. Here, we show that doublecortin-like kinase 1 (DCLK1) is upregulated after SCI in mice. Pharmacological inhibition of DCLK1 with DCLK1-IN-1 improved motor recovery, reduced glial scar formation and fibrosis, and preserved neurons at the lesion site. Mechanistically, we identified the microtubule-severing protein KATNA1 as a downstream target of DCLK1. DCLK1 directly phosphorylated KATNA1 at threonine 118 (T118), suppressing its microtubule-severing activity. DCLK1 overexpression inhibited, whereas DCLK1 knockdown or inhibition enhanced KATNA1 function. The T118D mutation reduced KATNA1 activity, while T118A resisted DCLK1-mediated suppression. In neurons, DCLK1 inhibited KATNA1-induced neurite outgrowth, whereas DCLK1 inhibition restored this effect.