Highlights
30• Based on the currently available genome sequence data, we proved that SARS-COV-2 genome has a much lower 31 mutation rate and genetic diversity than SARS during the 2002-2003 outbreak. 32• The spike (S) protein encoding gene of SARS-COV-2 is found relatively more conserved than other protein-encoding 33 genes, which is a good indication for the ongoing antiviral drug and vaccine development. 34• Minimum Evolution phylogeny analysis revealed the putative original status of SARS-CoV-2 and the early-stage 35 spread history. 36• We confirmed a previously reported rearrangement in the S protein arrangement of SARS-COV-2, and propose that 37 this rearrangement should have occurred between human SARS-CoV and a bat SARS-CoV, at a time point much 38 earlier before SARS-COV-2 transmission to human. 39• We provided first evidence that a mutated SARS-COV-2 with reduced human ACE2 receptor binding affinity have 40 emerged in India based on a sample collected on 27 th January 2020. 41 42 130 protein (Accession ID: YP_009724390.1). 131 132
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causal agent of COVID 19, continues to evolve since its first emergence in December 2019. Using the complete sequences of 1,932 SARS-CoV-2 genomes, various clustering analyses consistently identified six types of the strains. Independent of the dendrogram construction, 13 signature variations in the form of single nucleotide variations (SNVs) in protein coding regions and one SNV in the 5′ untranslated region (UTR) were identified and provided a direct interpretation for the six types (types I to VI). The six types of the strains and their underlying signature SNVs were validated in two subsequent analyses of 6,228 and 38,248 SARS-CoV-2 genomes which became available later. To date, type VI, characterized by the four signature SNVs C241T (5′UTR), C3037T (nsp3 F924F), C14408T (nsp12 P4715L), and A23403G (Spike D614G), with strong allelic associations, has become the dominant type. Since C241T is in the 5′ UTR with uncertain significance and the characteristics can be captured by the other three strongly associated SNVs, we focus on the other three. The increasing frequency of the type VI haplotype 3037T-14408T-23403G in the majority of the submitted samples in various countries suggests a possible fitness gain conferred by the type VI signature SNVs. The fact that strains missing one or two of these signature SNVs fail to persist implies possible interactions among these SNVs. Later SNVs such as G28881A, G28882A, and G28883C have emerged with strong allelic associations, forming new subtypes. This study suggests that SNVs may become an important consideration in SARS-CoV-2 classification and surveillance.
Enzyme-powered micro/nanomotors propelled
by biocompatible fuels
generally show a weak propulsive force, which greatly limits their
applications in complex biological environments. Herein, we have developed
a novel and versatile approach to significantly enhance the propulsion
of enzyme-powered micromotors by multilayered assembly of enzymes.
As an example, multilayers of biotinylated ureases (BU) were asymmetrically
immobilized on biotinylated Janus Au/magnetic microparticles (MMPs)
with the assistance of streptavidin (SA). When the mass ratio of BU
into SA and the amount of BU used in the assembly process are increased,
the amount of urease immobilized on the biotinylated Janus Au/MMPs
increased monotonously while the migration speed of the micromotor
was augmented gradually until a saturated value. The as-optimized
micromotors can be self-propelled with an average speed up to about
21.5 ± 0.8 μm/s at physiological urea concentrations (10
mM), which is five times faster than that of the monolayered counterparts
and two times faster than that of the previously reported values.
Owing to the enhanced thrust, the micromotors can move in liquids
with viscosities similar to that of blood. In addition, with the inherent
magnetic property of MMPs, the micromotors can exhibit fast magnetic
separation and controllable motion direction by external magnetic
fields. Our results provide a new pathway for designing high-efficient
enzyme-powered micro/nanomotors and thereby promote their biomedical
applications.
Mitochondrial DNAs (mtDNAs) from 167 American Indians including 87 Amerind-speakers (Amerinds) and 80 Nadene-speakers (Nadene) were surveyed for sequence variation by detailed restriction analysis. All Native American mtDNAs clustered into one of four distinct lineages, defined by the restriction site variants: HincII site loss at np 13,259, AluI site loss at np 5,176, 9-base pair (9-bp) COII-tRNA(Lys) intergenic deletion and HaeIII site gain at np 663. The HincII np 13,259 and AluI np 5,176 lineages were observed exclusively in Amerinds and were shared by all such tribal groups analyzed, thus demonstrating that North, Central and South American Amerinds originated from a common ancestral genetic stock. The 9-bp deletion and HaeIII np 663 lineages were found in both the Amerinds and Nadene but the Nadene HaeIII np 663 lineage had a unique sublineage defined by an RsaI site loss at np 16,329. The amount of sequence variation accumulated in the Amerind HincII np 13,259 and AluI np 5,176 lineages and that in the Amerind portion of the HaeIII np 663 lineage all gave divergence times in the order of 20,000 years before present. The divergence time for the Nadene portion of the HaeIII np 663 lineage was about 6,000-10,000 years. Hence, the ancestral Nadene migrated from Asia independently and considerably more recently than the progenitors of the Amerinds. The divergence times of both the Amerind and Nadene branches of the COII-tRNA(Lys) deletion lineage were intermediate between the Amerind and Nadene specific lineages, raising the possibility of a third source of mtDNA in American Indians.
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