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Three coronaviruses (CoVs) have threatened the world population by causing outbreaks in the last two decades. In late 2019, the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) emerged and caused the coronaviruses to disease 2019 (COVID-19), leading to the ongoing global outbreak. The other pandemic coronaviruses, SARS-CoV and Middle East respiratory syndrome CoV (MERS-CoV), share a considerable level of similarities at genomic and protein levels. However, the differences between them lead to distinct behaviors. These differences result from the accumulation of mutations in the sequence and structure of spike (S) glycoprotein, which plays an essential role in coronavirus infection, pathogenicity, transmission, and evolution. In this review, we brought together many studies narrating a sequence of events and highlighting the differences among S proteins from SARS-CoV, MERS-CoV, and SARS-CoV-2. It was performed here, analysis of S protein sequences and structures from the three pandemic coronaviruses pointing out the mutations among them and what they come through. Additionally, we investigated the receptor-binding domain (RBD) from all S proteins explaining the mutation and biological importance of all of them. Finally, we discuss the mutation in the S protein from several new isolates of SARS-CoV-2, reporting their difference and importance. This review brings into detail how the variations in S protein that make SARS-CoV-2 more aggressive than its relatives coronaviruses and other differences between coronaviruses.

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Endoplasmic reticulum (ER) stress is characterized by an accumulation of unfolded proteins induced by several adverse conditions, such as drought, salinity, and pathogens. Both tunicamycin (TM) and dithiothreitol (DTT) are applied to study the ER stress in plants. Although there is not a consensus of the concentration and chemicals used as well as physiological markers, it triggers the unfolded protein response (UPR) composed by sensors into the ER membrane, which start a signaling process to restore homeostasis or induce cell death. In this way, this review includes the advances in the knowledge of ER response induced by TM and DTT treatments, especially their downstream physiological effects. From low TM (≤ 0.5 µg ml-1) and DTT (0.5 to 1.0 mM) concentrations, the chlorophyll loss is linked to reactive oxygen species (ROS), and SA and JA signaling that result in growth impairment associated with UPR genes unbalance. Above 0.5 μg.ml-1 of TM or 1.0 mM DTT, a ROS cytoprotective role is crucial to stress acclimation or cell death. From 1.0 to 10 μg.ml-1 TM or 2.0 to 10 mM DTT, necrotic lesions are linked to electrolyte leakage, and fatty acid oxidation, which was more aggravated/intense at high concentration (50 and 200 μg.ml-1). Overall, this work associates crescent concentrations of two ER stressors and its downstream physiological responses, which helps to elucidate possible mechanisms to adjust to environmental stresses starting the mechanisms of adaptation to survival or death.