About 70% of the protein in isolated Bacillus subtilis spore coats was solubilized by treatment with a combination of reducing and denaturing agents at alkaline pH. The residue, consisting primarily of protein, was insoluble in a variety of reagents. The soluble proteins were resolved into at least seven bands by sodium dodecyl sulfate gel electrophoresis. About one-half of the total was four proteins of 8,000 to 12,000 daltons. These were relatively tyrosine rich, and one was a glycoprotein. There was also a cluster of proteins of about 40,000 daltons and two or three in the 20,000-to 25,000-dalton range. The insoluble fraction had an amino acid composition and N-terminal pattern of amino acids very similar to those of the soluble coat proteins. A major difference was the presence of considerable dityrosine in performic acid-oxidized preparations of insoluble coats. Coat antigen including a 60,000-dalton protein not present in extracts of mature spores was detected in extracts of sporulating cells by immunoprecipitation. This large antigen turned over in a pulse-chase experiment. Antibodies to either the array of 8,000-to 12,000-dalton coat polypeptides or to the larger coat proteins reacted with this 60,000-dalton species, suggesting a common precursor for many of the mature coat polypeptides. Spore coats seem to be assembled by processing ofproteins and by secondary modifications including perhaps dityrosine formation for cross-linking. The formation and assembly of the spore coat layers in Bacillus cereus begins early in sporulation and proceeds via synthesis and processing of a precursor (9, 32). These layers serve a protective function and perhaps have a role in germination (4-6, 10, 16, 32). 100 ,ug of lysozyme/ml. Lysis of vegetative cells with lysozyme was followed by one or two washings each with 1 M NaCl, 0.14 M NaCl, 0.1% (wt/vol) sodium dodecyl sulfate (SDS), 1 mM NaOH, and antibody buffer (9), followed by five washings with deionized water. Antibody buffer consisted of 0.05 M sodium

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) belongs to the group of Betacoronaviruses. The SARS-CoV-2 is closely related to SARS-CoV-1 and probably originated either from bats or pangolins. SARS-CoV-2 is an etiological agent of COVID-19, causing mild to severe respiratory disease which escalates to acute respiratory distress syndrome (ARDS) or multi-organ failure. The virus was first reported from the animal market in Hunan, Hubei province of China in the month of December, 2019, and was rapidly transmitted from animal to human and human-to-human. The human-to-human transmission can occur directly or via droplets generated during coughing and sneezing. Globally, around 53.9 million cases of COVID-19 have been registered with 1.31 million confirmed deaths. The people > 60 years, persons suffering from comorbid conditions and immunocompromised individuals are more susceptible to COVID-19 infection. The virus primarily targets the upper and the lower respiratory tract and quickly disseminates to other organs. SARS-CoV-2 dysregulates immune signaling pathways which generate cytokine storm and leads to the acute respiratory distress syndrome and other multisystemic disorders.

In agriculture, heat stress (HS) has become one of the eminent abiotic threats to crop growth, productivity and nutritional security because of the continuous increase in global mean temperature. Studies have annotated that the heat stress response (HSR) in plants is highly conserved, involving complex regulatory networks of various signaling and sensor molecules. In this context, the ubiquitous‐signaling molecules salicylic acid (SA) and nitric oxide (NO) have diverted the attention of the plant science community because of their putative roles in plant abiotic and biotic stress tolerance. However, their involvement in the transcriptional regulatory networks in plant HS tolerance is still poorly understood. In this review, we have conceptualized current knowledge concerning how SA and NO sense HS in plants and how they trigger the HSR leading to the activation of transcriptional‐signaling cascades. Fundamentals of functional components and signaling networks associated with molecular mechanisms involved in SA/NO‐mediated HSR in plants have also been discussed. Increasing evidences have suggested the involvement of epigenetic modifications in the development of a ‘stress memory’, thereby provoking the role of epigenetic mechanisms in the regulation of plant's innate immunity under HS. Thus, we have also explored the recent advancements regarding the biological mechanisms and the underlying significance of epigenetic regulations involved in the activation of HS responsive genes and transcription factors by providing conceptual frameworks for understanding molecular mechanisms behind the ‘transcriptional stress memory’ as potential memory tools in the regulation of plant HSR.