Hox genes code for transcription factors and are evolutionarily conserved. They regulate a plethora of downstream targets to define the anterior-posterior (AP) body axis of a developing bilaterian embryo. Early work suggested a possible role of clustering and ordering of Hox to regulate their expression in a spatially restricted manner along the AP axis. However, the recent availability of many genome assemblies for different organisms uncovered several examples that defy this constraint. With recent advancements in genomics, the current review discusses the arrangement of Hox in various organisms. Further, we revisit their discovery and regulation in Drosophila melanogaster. We also review their regulation in different arthropods and vertebrates, with a significant focus on Hox expression in the crustacean Parahyale hawaiensis. It is noteworthy that subtle changes in the levels of Hox gene expression can contribute to the development of novel features in an organism. We, therefore, delve into the distinct regulation of these genes during primary axis formation, segment identity, and extra-embryonic roles such as in the formation of hair follicles or misregulation leading to cancer. Toward the end of each section, we emphasize the possibilities of several experiments involving various organisms, owing to the advancements in the field of genomics and CRISPR-based genome engineering. Overall, we present a holistic view of the functioning of Hox in the animal world.

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Dear Editor,COVID-19 has an extremely variable prognosis, ranging from asymptomatic and mildly affected individuals to severe disease and death. We have investigated the transcriptional changes in 36 COVID-19 positive Indian patients hospitalized during the first surge (Figure 1A, Table S1, and Supplementary Methods) against 5 COVID-19 negative samples. RNA was isolated from naso/oropharyngeal swabs for paired end sequencing using the Illumina Nova-seq 6000. We identified 251 upregulated (220 protein coding) and 9068 downregulated (3252 protein coding) differentially expressed genes (DEGs) (adjusted p-value < 0.05 and absolute log2 fold change > 1) (Figure 1B, Tables S2 and S3). Seven patients were critical and required intensive care unit (ICU) intervention, while 23 were discharged from COVID-19 ward (W), although no significant differences could be seen in their transcriptional profiles (Figure 1C). The overall transcriptional reduction, irrespective of disease severity (Figure 1C), is well correlated with the phenomenon of fading host cell functionality and prominent viral protein synthesis, and may be associated with interference in host cellular processes and responses. 1 The results indicate a diverse transcriptomic profile in response to SARS-CoV-2, in line with the variable prognosis seen in many COVID-19 patients. However, we find robust activation of the innate immune response concomitant with a reduction in the gene expression profiles associated with cardiac, muscular, and neurological processes, as well as peripheral neurosensory markers.Immune response genes were highly upregulated (Figure 2A and Table S4), with prominent clusters of genes associated with multiple viral infections (Figure 2B and Table S5) marking the activation of infection clearance pathways. Meta-analysis of published datasets identified a signature of 19 upregulated genes (Table S6), linking Type I interferon (IFN) signaling, host defense, and innate immune responses in SARS-CoV-2 infection (Fig-This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Background: One of the most perplexing aspects of infection with the SARS-CoV-2 virus has been the variable response elicited in its human hosts. Investigating the transcriptional changes in individuals affected by COVID-19 can help understand and predict the degree of illness and guide clinical outcomes in diverse backgrounds. Methods: Analysis of host transcriptome variations via RNA sequencing from naso/oropharyngeal swabs of COVID-19 patients. Results: We report strong upregulation of the innate immune response, especially type I interferon pathway, upon SARS-CoV-2 infection. Upregulated genes were subjected to a comparative meta-analysis using global datasets to identify a common network of interferon stimulated and viral response genes that mediate the host response and resolution of infection. A large proportion of mis-regulated genes showed a reduction in expression level, suggesting an overall decrease in host mRNA production. Significantly downregulated genes included those encoding olfactory, taste and neuro-sensory receptors. Many pro-inflammatory markers and cytokines were also downregulated or remained unchanged in the COVID-19 patients. Finally, a large number of non-coding RNAs were identified as down-regulated, with a few of the lncRNAs associated with functional roles in directing the response to viral infection. Conclusions: SARS-CoV-2 infection results in the robust activation of the innate immunity. Reduction of gene expression is well correlated with the clinical manifestations and symptoms of COVID-19 such as the loss of smell and taste, and myocardial and neurological complications. This study provides a critical dataset of genes that will enhance our understanding of the nature and prognosis of COVID-19.