scholarly journals Loss of Spike N370 glycosylation as an important evolutionary event for the enhanced infectivity of SARS-CoV-2

Cell Research ◽  
2022 ◽  
Author(s):  
Shuyuan Zhang ◽  
Qingtai Liang ◽  
Xinheng He ◽  
Chongchong Zhao ◽  
Wenlin Ren ◽  
...  
Keyword(s):  
PalZ ◽  
2021 ◽  
Author(s):  
Xingliang Zhang ◽  
Degan Shu

AbstractThe Cambrian Explosion by nature is a three-phased explosion of animal body plans alongside episodic biomineralization, pulsed change of generic diversity, body size variation, and progressive increase of ecosystem complexity. The Cambrian was a time of crown groups nested by numbers of stem groups with a high-rank taxonomy of Linnaean system (classes and above). Some stem groups temporarily succeeded while others were ephemeral and underrepresented by few taxa. The high number of stem groups in the early history of animals is a major reason for morphological gaps across phyla that we see today. Most phylum-level clades achieved their maximal disparity (or morphological breadth) during the time interval close to their first appearance in the fossil record during the early Cambrian, whereas others, principally arthropods and chordates, exhibit a progressive exploration of morphospace in subsequent Phanerozoic. The overall envelope of metazoan morphospace occupation was already broad in the early Cambrian though it did not reach maximal disparity nor has diminished significantly as a consequence of extinction since the Cambrian. Intrinsic and extrinsic causes were extensively discussed but they are merely prerequisites for the Cambrian Explosion. Without the molecular evolution, there could be no Cambrian Explosion. However, the developmental system is alone insufficient to explain Cambrian Explosion. Time-equivalent environmental changes were often considered as extrinsic causes, but the time coincidence is also insufficient to establish causality. Like any other evolutionary event, it is the ecology that make the Cambrian Explosion possible though ecological processes failed to cause a burst of new body plans in the subsequent evolutionary radiations. The Cambrian Explosion is a polythetic event in natural history and manifested in many aspects. No simple, single cause can explain the entire phenomenon.


2016 ◽  
Vol 198 (6) ◽  
pp. 994-1004 ◽  
Author(s):  
Arup Dey ◽  
Christopher N. Vassallo ◽  
Austin C. Conklin ◽  
Darshankumar T. Pathak ◽  
Vera Troselj ◽  
...  

ABSTRACTMyxobacteria form complex social communities that elicit multicellular behaviors. One such behavior is kin recognition, in which cells identify siblings via their polymorphic TraA cell surface receptor, to transiently fuse outer membranes and exchange their contents. In addition, outer membrane exchange (OME) regulates behaviors, such as inhibition of wild-typeMyxococcus xanthus(DK1622) from swarming. Here we monitored the fate of motile cells and surprisingly found they were killed by nonmotile siblings. The kill phenotype required OME (i.e., was TraA dependent). The genetic basis of killing was traced to ancestral strains used to construct DK1622. Specifically, the kill phenotype mapped to a large “polyploid prophage,” Mx alpha. Sensitive strains contained a 200-kb deletion that removed two of three Mx alpha units. To explain these results, we suggest that Mx alpha expresses a toxin-antitoxin cassette that uses the OME machinery ofM. xanthusto transfer a toxin that makes the population “addicted” to Mx alpha. Thus, siblings that lost Mx alpha units (no immunity) are killed by cells that harbor the element. To test this, an Mx alpha-harboring laboratory strain was engineered (bytraAallele swap) to recognize a closely related species,Myxococcus fulvus. As a result,M. fulvus, which lacks Mx alpha, was killed. These TraA-mediated antagonisms provide an explanation for how kin recognition specificity might have evolved in myxobacteria. That is, recognition specificity is determined by polymorphisms intraA, which we hypothesize were selected for because OME with non-kin leads to lethal outcomes.IMPORTANCEThe transition from single cell to multicellular life is considered a major evolutionary event. Myxobacteria have successfully made this transition. For example, in response to starvation, individual cells aggregate into multicellular fruiting bodies wherein cells differentiate into spores. To build fruits, cells need to recognize their siblings, and in part, this is mediated by the TraA cell surface receptor. Surprisingly, we report that TraA recognition can also involve sibling killing. We show that killing originates from a prophage-like element that has apparently hijacked the TraA system to deliver a toxin to kin. We hypothesize that this killing system has imposed selective pressures on kin recognition, which in turn has resulted in TraA polymorphisms and hence many different recognition groups.


2005 ◽  
Vol 95 (2) ◽  
pp. 128-135 ◽  
Author(s):  
Tetsuo Maoka ◽  
Tatsuji Hataya

The complete nucleotide sequence of the genome of Papaya leaf distortion mosaic virus (PLDMV) was determined. The viral RNA genome of strain LDM (leaf distortion mosaic) comprised 10,153 nucleotides, excluding the poly(A) tail, and contained one long open reading frame encoding a polyprotein of 3,269 amino acids (molecular weight 373,347). The polyprotein contained nine putative proteolytic cleavage sites and some motifs conserved in other potyviral polyproteins with 44 to 50% identities, indicating that PLDMV is a distinct species in the genus Potyvirus. Like the W biotype of Papaya ringspot virus (PRSV), the non-papaya-infecting biotype of PLDMV (PLDMV-C) was found in plants of the family Cucurbitaceae. The coat protein (CP) sequence of PLDMV-C in naturally infected-Trichosanthes bracteata was compared with those of three strains of the P biotype (PLDMV-P), LDM and two additional strains M (mosaic) and YM (yellow mosaic), which are biologically different from each other. The CP sequences of three strains of PLDMV-P share high identities of 95 to 97%, while they share lower identities of 88 to 89% with that of PLDMV-C. Significant changes in hydrophobicity and a deletion of two amino acids at the N-terminal region of the CP of PLDMV-C were observed. The finding of two biotypes of PLDMV implies the possibility that the papaya-infecting biotype evolved from the cucurbitaceae-infecting potyvirus, as has been previously suggested for PRSV. In addition, a similar evolutionary event acquiring infectivity to papaya may arise frequently in viruses in the family Cucurbitaceae.


2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Di Sun ◽  
Xuming Zhou ◽  
Zhenpeng Yu ◽  
Shixia Xu ◽  
Inge Seim ◽  
...  

Abstract Background The transition from land to sea by the ancestor of cetaceans approximately 50 million years ago was an incredible evolutionary event that led to a series of morphological, physiological, and behavioral adaptations. During this transition, bone microstructure evolved from the typical terrestrial form to the specialized structure found in modern cetaceans. While the bone microstructure of mammals has been documented before, investigations of its genetic basis lag behind. The increasing number of cetaceans with whole-genome sequences available may shed light on the mechanism underlying bone microstructure evolution as a result of land to water transitions. Results Cetacean bone microstructure is consistent with their diverse ecological behaviors. Molecular evolution was assessed by correlating bone microstructure and gene substitution rates in terrestrial and aquatic species, and by detecting genes under positive selection along ancestral branches of cetaceans. We found that: 1) Genes involved in osteoclast function are under accelerated evolution in cetaceans, suggestive of important roles in bone remodeling during the adaptation to an aquatic environment; 2) Genes in the Wnt pathway critical for bone development and homeostasis show evidence of divergent evolution in cetaceans; 3) Several genes encoding bone collagens are under selective pressure in cetaceans. Conclusions Our results suggest that evolutionary pressures have shaped the bone microstructure of cetaceans, to facilitate life in diverse aquatic environments.


2017 ◽  
Vol 199 (13) ◽  
Author(s):  
Jessica M. Gullett ◽  
Amber Bible ◽  
Gladys Alexandre

ABSTRACT Chemotaxis is the movement of cells in response to gradients of diverse chemical cues. Motile bacteria utilize a conserved chemotaxis signal transduction system to bias their motility and navigate through a gradient. A central regulator of chemotaxis is the histidine kinase CheA. This cytoplasmic protein interacts with membrane-bound receptors, which assemble into large polar arrays, to propagate the signal. In the alphaproteobacterium Azospirillum brasilense, Che1 controls transient increases in swimming speed during chemotaxis, but it also biases the cell length at division. However, the exact underlying molecular mechanisms for Che1-dependent control of multiple cellular behaviors are not known. Here, we identify specific domains of the CheA1 histidine kinase implicated in modulating each of these functions. We show that CheA1 is produced in two isoforms: a membrane-anchored isoform produced as a fusion with a conserved seven-transmembrane domain of unknown function (TMX) at the N terminus and a soluble isoform similar to prototypical CheA. Site-directed and deletion mutagenesis combined with behavioral assays confirm the role of CheA1 in chemotaxis and implicate the TMX domain in mediating changes in cell length. Fluorescence microscopy further reveals that the membrane-anchored isoform is distributed around the cell surface while the soluble isoform localizes at the cell poles. Together, the data provide a mechanism for the role of Che1 in controlling multiple unrelated cellular behaviors via acquisition of a new domain in CheA1 and production of distinct functional isoforms. IMPORTANCE Chemotaxis provides a significant competitive advantage to bacteria in the environment, and this function has been transferred laterally multiple times, with evidence of functional divergence in different genomic contexts. The molecular principles that underlie functional diversification of chemotaxis in various genomic contexts are unknown. Here, we provide a molecular mechanism by which a single CheA protein controls two unrelated functions: chemotaxis and cell length. Acquisition of this multifunctionality is seemingly a recent evolutionary event. The findings illustrate a mechanism by which chemotaxis function may be co-opted to regulate additional cellular functions.


2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Irina V. Poverennaya ◽  
Nadezhda A. Potapova ◽  
Sergey A. Spirin

Abstract Background Eukaryotic protein-coding genes consist of exons and introns. Exon–intron borders are conserved between species and thus their changes might be observed only on quite long evolutionary distances. One of the rarest types of change, in which intron relocates over a short distance, is called "intron sliding", but the reality of this event has been debated for a long time. The main idea of a search for intron sliding is to use the most accurate genome annotation and genome sequence, as well as high-quality transcriptome data. We applied them in a search for sliding introns in mammals in order to widen knowledge about the presence or absence of such phenomena in this group. Results We didn’t find any significant evidence of intron sliding in the primate group (human, chimpanzee, rhesus macaque, crab-eating macaque, green monkey, marmoset). Only one possible intron sliding event supported by a set of high quality transcriptomes was observed between EIF1AX human and sheep gene orthologs. Also, we checked a list of previously observed intron sliding events in mammals and showed that most likely they are artifacts of genome annotations and are not shown in subsequent annotation versions as well as are not supported by transcriptomic data. Conclusions We assume that intron sliding is indeed a very rare evolutionary event if it exists at all. Every case of intron sliding needs a lot of supportive data for detection and confirmation.


2018 ◽  
Vol 5 (11) ◽  
pp. 180879 ◽  
Author(s):  
Hiroki Koda ◽  
Takumi Kunieda ◽  
Takeshi Nishimura

Voluntary control of vocal production is an essential component of the language faculty, which is thought to distinguish humans from other primates. Recent experiments have begun to reveal the capability of non-human primates to perform vocal control; however, the mechanisms underlying this ability remain unclear. Here, we revealed that Japanese macaque monkeys can learn to vocalize voluntarily through a different mechanism than that used for manual actions. The monkeys rapidly learned to touch a computer monitor when a visual stimulus was presented and showed a capacity for flexible adaptation, such that they reacted when the visual stimulus was shown at an unexpected time. By contrast, successful vocal training required additional time, and the monkeys exhibited difficulty with vocal execution when the visual stimulus appeared earlier than expected; this occurred regardless of extensive training. Thus, motor preparation before execution of an action may be a key factor in distinguishing vocalization from manual actions in monkeys; they do not exhibit a similar ability to perform motor preparation in the vocal domains. By performing direct comparisons, this study provides novel evidence regarding differences in motor control abilities between vocal and manual actions. Our findings support the suggestion that the functional expansion from hand to mouth might be a critical evolutionary event for the acquisition of voluntary control of vocalizations.


1988 ◽  
Vol 66 (2) ◽  
pp. 257-271 ◽  
Author(s):  
Elisa D'Antoni D'Amelio ◽  
Eduardo Zeiger

Guard cells of species representing 27 genera from the Orchidaceae were surveyed under fluorescence microscopy. With the exception of the genus Paphiopedilum, chlorophyll a fluorescence was observed in all species, indicating that, as in other families, chloroplasts are strongly conserved in the stomata of the Orchidaceae. The achlorophyllous stomata of Paphiopedilum therefore constitute a unique variation in that pattern, with its expression at the generic level pointing to an early, stable evolutionary event. Five of the orchid species, Vanilla aromaticum, Phragmipedium longifolium, Haemaria discolor, Paphiopedilum harrisianum, and Paphiopedilum insigne, were also studied ultrastructurally. There was a close correlation between plastid fluorescence intensity in guard cells and the presence of grana thylakoids in the organelles, with Vanilla showing an intense fluorescence and extensive grana stacking, while the Paphiopedilum stomata were completely devoid of both features. Phragmipedium stomata had an intermediate level of fluorescence and a reduced number of thylakoids, whereas Haemaria guard cells, which had no chlorophyll fluorescence in intact tissue but a weak fluorescence in cryostat sections, showed an unusual array of pleomorphic plastids with only a few exhibiting some thylakoids. Other ultrastructural features of orchid guard cells were also documented. These observations and a marked variation in fluorescence intensity and plastid number and size seen in the guard cells of the surveyed genera point to a broad structural diversity in the guard cell plastids of the Orchidaceae. This diversity could underlie specialized functional properties associated with stomatal adaptations to different growing habitats.


Author(s):  
Adnan Saeed Amin

No single evolutionary event has been identified as the cause for the final emergence of our species. I propose that a mutation on CD155 receptor gene occurred to establish a symbiosis with poliovirus, which exerted its beneficial impact via RNA dependent non-genetic transgenerational inheritance, which caused a qualitative enhancement of cognitive functions. I posit that this mutation occurred in what we call, Anatomically Modern Humans, our immediate ancestor species and that the disruption of this symbiosis causes autism spectrum disorder. Positive selection of CD155 to the extent of becoming a species defining characteristic, the chronology of autism spectrum disorder prevalence increase and continued increase, the multigenerational nature of RNA inheritance, the universal infection of humans by poliovirus and a very low associated mortality rate, and several other factors support this hypothesis. Specific genetic, epidemiological and sperm miRNA content studies are suggested to test this hypothesis.


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