@article{14783, abstract = {Connexin 43, an astroglial gap junction protein, is enriched in perisynaptic astroglial processes and plays major roles in synaptic transmission. We have previously found that astroglial Cx43 controls synaptic glutamate levels and allows for activity-dependent glutamine release to sustain physiological synaptic transmissions and cognitiogns. However, whether Cx43 is important for the release of synaptic vesicles, which is a critical component of synaptic efficacy, remains unanswered. Here, using transgenic mice with a glial conditional knockout of Cx43 (Cx43−/−), we investigate whether and how astrocytes regulate the release of synaptic vesicles from hippocampal synapses. We report that CA1 pyramidal neurons and their synapses develop normally in the absence of astroglial Cx43. However, a significant impairment in synaptic vesicle distribution and release dynamics were observed. In particular, the FM1-43 assays performed using two-photon live imaging and combined with multi-electrode array stimulation in acute hippocampal slices, revealed a slower rate of synaptic vesicle release in Cx43−/− mice. Furthermore, paired-pulse recordings showed that synaptic vesicle release probability was also reduced and is dependent on glutamine supply via Cx43 hemichannel (HC). Taken together, we have uncovered a role for Cx43 in regulating presynaptic functions by controlling the rate and probability of synaptic vesicle release. Our findings further highlight the significance of astroglial Cx43 in synaptic transmission and efficacy.}, author = {Cheung, Giselle T and Chever, Oana and Rollenhagen, Astrid and Quenech’du, Nicole and Ezan, Pascal and Lübke, Joachim H. R. and Rouach, Nathalie}, issn = {2073-4409}, journal = {Cells}, keywords = {General Medicine}, number = {8}, publisher = {MDPI}, title = {{Astroglial connexin 43 regulates synaptic vesicle release at hippocampal synapses}}, doi = {10.3390/cells12081133}, volume = {12}, year = {2023}, } @article{13214, abstract = {Nitrogen is an important macronutrient required for plant growth and development, thus directly impacting agricultural productivity. In recent years, numerous studies have shown that nitrogen-driven growth depends on pathways that control nitrate/nitrogen homeostasis and hormonal networks that act both locally and systemically to coordinate growth and development of plant organs. In this review, we will focus on recent advances in understanding the role of the plant hormones auxin and cytokinin and their crosstalk in nitrate-regulated growth and discuss the significance of novel findings and possible missing links.}, author = {Abualia, R and Riegler, Stefan and Benková, Eva}, issn = {2073-4409}, journal = {Cells}, number = {12}, publisher = {MDPI}, title = {{Nitrate, auxin and cytokinin - a trio to tango}}, doi = {10.3390/cells12121613}, volume = {12}, year = {2023}, } @article{10015, abstract = {Auxin plays a dual role in growth regulation and, depending on the tissue and concentration of the hormone, it can either promote or inhibit division and expansion processes in plants. Recent studies have revealed that, beyond transcriptional reprogramming, alternative auxincontrolled mechanisms regulate root growth. Here, we explored the impact of different concentrations of the synthetic auxin NAA that establish growth-promoting and -repressing conditions on the root tip proteome and phosphoproteome, generating a unique resource. From the phosphoproteome data, we pinpointed (novel) growth regulators, such as the RALF34-THE1 module. Our results, together with previously published studies, suggest that auxin, H+-ATPases, cell wall modifications and cell wall sensing receptor-like kinases are tightly embedded in a pathway regulating cell elongation. Furthermore, our study assigned a novel role to MKK2 as a regulator of primary root growth and a (potential) regulator of auxin biosynthesis and signalling, and suggests the importance of the MKK2 Thr31 phosphorylation site for growth regulation in the Arabidopsis root tip.}, author = {Nikonorova, N and Murphy, E and Fonseca de Lima, CF and Zhu, S and van de Cotte, B and Vu, LD and Balcerowicz, D and Li, Lanxin and Kong, X and De Rop, G and Beeckman, T and Friml, Jiří and Vissenberg, K and Morris, PC and Ding, Z and De Smet, I}, issn = {2073-4409}, journal = {Cells}, keywords = {primary root, (phospho)proteomics, auxin, (receptor) kinase}, publisher = {MDPI}, title = {{The Arabidopsis root tip (phospho)proteomes at growth-promoting versus growth-repressing conditions reveal novel root growth regulators}}, doi = {10.3390/cells10071665}, volume = {10}, year = {2021}, } @article{8949, abstract = {Development of the nervous system undergoes important transitions, including one from neurogenesis to gliogenesis which occurs late during embryonic gestation. Here we report on clonal analysis of gliogenesis in mice using Mosaic Analysis with Double Markers (MADM) with quantitative and computational methods. Results reveal that developmental gliogenesis in the cerebral cortex occurs in a fraction of earlier neurogenic clones, accelerating around E16.5, and giving rise to both astrocytes and oligodendrocytes. Moreover, MADM-based genetic deletion of the epidermal growth factor receptor (Egfr) in gliogenic clones revealed that Egfr is cell autonomously required for gliogenesis in the mouse dorsolateral cortices. A broad range in the proliferation capacity, symmetry of clones, and competitive advantage of MADM cells was evident in clones that contained one cellular lineage with double dosage of Egfr relative to their environment, while their sibling Egfr-null cells failed to generate glia. Remarkably, the total numbers of glia in MADM clones balance out regardless of significant alterations in clonal symmetries. The variability in glial clones shows stochastic patterns that we define mathematically, which are different from the deterministic patterns in neuronal clones. This study sets a foundation for studying the biological significance of stochastic and deterministic clonal principles underlying tissue development, and identifying mechanisms that differentiate between neurogenesis and gliogenesis.}, author = {Zhang, Xuying and Mennicke, Christine V. and Xiao, Guanxi and Beattie, Robert J and Haider, Mansoor and Hippenmeyer, Simon and Ghashghaei, H. Troy}, issn = {2073-4409}, journal = {Cells}, number = {12}, publisher = {MDPI}, title = {{Clonal analysis of gliogenesis in the cerebral cortex reveals stochastic expansion of glia and cell autonomous responses to Egfr dosage}}, doi = {10.3390/cells9122662}, volume = {9}, year = {2020}, }