The fungal cell wall confers cell morphology and protection against environmental insults. For fungal pathogens, the cell wall is a key immunological modulator and an ideal therapeutic target. Yeast cell walls possess an inner matrix of interlinked β-glucan and chitin that is thought to provide tensile strength and rigidity. Yeast cells remodel their walls over time in response to environmental change, a process controlled by evolutionarily conserved stress (Hog1) and cell integrity (Mkc1, Cek1) signaling pathways. These mitogen-activated protein kinase (MAPK) pathways modulate cell wall gene expression, leading to the construction of a new, modified cell wall. We show that the cell wall is not rigid but elastic, displaying rapid structural realignments that impact survival following osmotic shock. Lactate-grown Candida albicans cells are more resistant to hyperosmotic shock than glucose-grown cells. We show that this elevated resistance is not dependent on Hog1 or Mkc1 signaling and that most cell death occurs within 10 min of osmotic shock. Sudden decreases in cell volume drive rapid increases in cell wall thickness. The elevated stress resistance of lactate-grown cells correlates with reduced cell wall elasticity, reflected in slower changes in cell volume following hyperosmotic shock. The cell wall elasticity of lactate-grown cells is increased by a triple mutation that inactivates the Crh family of cell wall cross-linking enzymes, leading to increased sensitivity to hyperosmotic shock. Overexpressing Crh family members in glucose-grown cells reduces cell wall elasticity, providing partial protection against hyperosmotic shock. These changes correlate with structural realignment of the cell wall and with the ability of cells to withstand osmotic shock. IMPORTANCE The C. albicans cell wall is the first line of defense against external insults, the site of immune recognition by the host, and an attractive target for antifungal therapy. Its tensile strength is conferred by a network of cell wall polysaccharides, which are remodeled in response to growth conditions and environmental stress. However, little is known about how cell wall elasticity is regulated and how it affects adaptation to stresses such as sudden changes in osmolarity. We show that elasticity is critical for survival under conditions of osmotic shock, before stress signaling pathways have time to induce gene expression and drive glycerol accumulation. Critical cell wall remodeling enzymes control cell wall flexibility, and its regulation is strongly dependent on host nutritional inputs. We also demonstrate an entirely new level of cell wall dynamism, where significant architectural changes and structural realignment occur within seconds of an osmotic shock.

Perturbations of the yeast cell wall trigger a repair mechanism that reconfigures its molecular structure to preserve cell integrity. To investigate this mechanism, we compared the global gene expression in five mutant strains, each bearing a mutation (i.e. fks1, kre6, mnn9, gas1, and knr4 mutants) that affects in a different manner the cell wall construction. Altogether, 300 responsive genes were kept based on high stringency criteria during data processing. Functional classification of these differentially expressed genes showed a substantial subset of induced genes involved in cell wall construction and an enrichment of metabolic, energy generation, and cell defense categories, whereas families of genes belonging to transcription, protein synthesis, and cellular growth were underrepresented. Clustering methods isolated a single group of ∼80 up-regulated genes that could be considered as the stereotypical transcriptional response of the cell wall compensatory mechanism. The in silico analysis of the DNA upstream region of these co-regulated genes revealed pairwise combinations of DNA-binding sites for transcriptional factors implicated in stress and heat shock responses (Msn2/4p and Hsf1p) with Rlm1p and Swi4p, two PKC1-regulated transcription factors involved in the activation genes related to cell wall biogenesis and G₁/S transition. Moreover, this computational analysis also uncovered the 6-bp 5′-AGCCTC-3′ CDRE (calcineurin-dependent response element) motif in 40% of the co-regulated genes. This motif was recently shown to be the DNA binding site for Crz1p, the major effector of calcineurin-regulated gene expression in yeast. Taken altogether, the data presented here lead to the conclusion that the cell wall compensatory mechanism, as triggered by cell wall mutations, integrates three major regulatory systems: namely the PKC1-SLT2 mitogen-activated protein kinase-signaling module, the “global stress” response mediated by Msn2/4p, and the Ca²⁺/calcineurin-dependent pathway. The relative importance of these regulatory systems in the cell wall compensatory mechanism is discussed.

In catalytic industrial processes, coke deposition remains a major drawback for solid catalysts use as it causes catalyst deactivation. Extensive study of this phenomenon over the last decades has provided a better understanding of coke behavior in a great number of processes. Among them, catalytic pyrolysis of plastics, which has been identified as a promising process for waste revalorization, is given particular attention in this paper. Combined economic and environmental concerns rose the necessity to restore catalytic activity by recovering deactivated catalysts. Consequently, various regeneration processes have been investigated over the years and development of an efficient and sustainable process remains an industrial challenge. Coke removal can be achieved via several chemical processes, such as oxidation, gasification, and hydrogenation. This review focuses on oxidative treatments for catalyst regeneration, covering the current progress of oxidation treatments and presenting advantages and drawbacks for each method. Molecular oxidation with oxygen and ozone, as well as advanced oxidation processes with the formation of OH radicals, are detailed to provide a deep understanding of the mechanisms and kinetics involved (direct and indirect oxidation, reaction rates and selectivity, diffusion, and mass transfer). Finally, this paper summarizes all relevant analytical techniques that can be used to characterize deactivated and regenerated solid catalysts: XRD, N₂ adsorption-desorption, SEM, NH₃-TPD, elemental analysis, IR. Analytical techniques are classified according to the type of information they provide, such as structural characteristics, elemental composition, or chemical properties. In function of the investigated property, this overall tool is useful and easy-to-use to determine the adequate analysis.