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Background The Indian peafowl ( Pavo cristanus ) is native to South Asia and is the national bird of India. Here we present a draft genome sequence of the male blue peacock using Illumina and Oxford Nanopore technology (ONT). Results ONT sequencing gave ∼2.3-fold sequencing coverage, whereas Illumina generated 150–base pair paired-end sequence data at 284.6-fold coverage from 5 libraries. Subsequently, we generated a 0.915-gigabase pair de novo assembly of the peacock genome with a scaffold N50 of 0.23 megabase pairs (Mb). We predict that the peacock genome contains 23,153 protein-coding genes and 75.3 Mb (7.33%) of repetitive sequences. Conclusions We report a high-quality assembly of the peacock genome using a hybrid approach of sequences generated by both Illumina and ONT. The long-read chemistry generated by ONT was useful for addressing challenges related to de novo assembly, particularly at regions containing repetitive sequences spanning longer than the read length, and which could not be resolved with only short-read–based assembly. Contig assembly of Illumina short reads gave an N50 of 1,639 bases, whereas with ONT, the N50 increased by >9-fold to 14,749 bases. The initial contig assembly based on Illumina sequencing reads alone gave 685,241 contigs. Further scaffolding on assembled contigs using both Illumina and ONT sequencing reads resulted in a final assembly of 15,025 super-scaffolds, with an N50 of ∼0.23 Mb. Ninety-five percent of proteins predicted by homology matched with those in a public repository, verifying the completeness of our assembly. Like other phylogenetic studies of avian conserved genes, we found P. cristatus to be most closely related to Gallus gallus , followed by Meleagris gallopavo and Anas platyrhynchos . Compared with the recently published peacock genome assembly, the current, superior, hybrid assembly has greater sequencing depth, fewer non-ATGC sequences, and fewer scaffolds.

Background Though a large number of pregnant females have been affected by COVID-19, there is a dearth of information on the effects of SARS-CoV-2 infection on trophoblast function. We explored in silico , the potential interactions between SARS-CoV-2 proteins and proteins involved in the key functions of placenta. Methods Human proteins interacting with SARS-CoV-2 proteins were identified by Gordon et al. (2020). Genes that are upregulated in trophoblast sub-types and stages were obtained by gene-expression data from NCBI-GEO and by text-mining. Genes altered in pathological states like pre-eclampsia and gestational diabetes mellitus were also identified. Genes crucial in placental functions thus identified were compared to the SARS-CoV-2 interactome for overlaps. Proteins recurring across multiple study scenarios were analyzed using text mining and network analysis for their biological functions. Results The entry receptors for SARS-CoV-2 – ACE2 and TMPRSS2 are expressed in placenta. Other proteins that interact with SARS-CoV-2 like LOX, Fibulins-2 and 5, NUP98, GDF15, RBX1, CUL3, HMOX1, PLAT, MFGE8, and MRPs are vital in placental functions like trophoblast invasion and migration, syncytium formation, differentiation, and implantation. TLE3, expressed across first trimester placental tissues and cell lines, is involved in formation of placental vasculature, and is important in SARS-CoV (2003) budding and exit from the cells by COPI vesicles. Conclusion SARS-CoV-2 can potentially interact with proteins having crucial roles in the placental function. Whether these potential interactions identified in silico have effects on trophoblast functions in biological settings needs to be addressed by further in vitro and clinical studies.

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Cancer stem cells (CSC) are the minor population of cancer originating cells that have the capacity of self-renewal, differentiation, and tumorigenicity (when transplanted into an immunocompromised animal). These low-copy number cell populations are believed to be resistant to conventional chemo and radiotherapy. It was reported that metabolic adaptation of these elusive cell populations is to a large extent responsible for their survival and distant metastasis. Warburg effect is a hallmark of most cancer in which the cancer cells prefer to metabolize glucose anaerobically, even under normoxic conditions. Warburg’s aerobic glycolysis produces ATP efficiently promoting cell proliferation by reprogramming metabolism to increase glucose uptake and stimulating lactate production. This metabolic adaptation also seems to contribute to chemoresistance and immune evasion, a prerequisite for cancer cell survival and proliferation. Though we know a lot about metabolic fine-tuning in cancer, what is still in shadow is the identity of upstream regulators that orchestrates this process. Epigenetic modification of key metabolic enzymes seems to play a decisive role in this. By altering the metabolic flux, cancer cells polarize the biochemical reactions to selectively generate “onco-metabolites” that provide an added advantage for cell proliferation and survival. In this review, we explored the metabolic-epigenetic circuity in relation to cancer growth and proliferation and establish the fact how cancer cells may be addicted to specific metabolic pathways to meet their needs. Interestingly, even the immune system is re-calibrated to adapt to this altered scenario. Knowing the details is crucial for selective targeting of cancer stem cells by choking the rate-limiting stems and crucial branch points, preventing the formation of onco-metabolites.