The evolution of neurosensation drives the gain and loss of phenotypic plasticity

Phenotypic plasticity is widely regarded as important for enabling species resilience to environmental change and for species evolution. However, insight into the complex mechanisms by which phenotypic plasticity evolves in nature has been limited by our ability to reconstruct evolutionary histories of plasticity. By using part of the molecular mechanism, we were able to trace the evolution of pre-feeding phenotypic plasticity across the class Echinoidea and identify the origin of plasticity at the base of the regular urchins. The neurosensory foundation for plasticity was ancestral within the echinoids. However, coincident development of the plastic trait and the neurosensory system was not achieved until the regular urchins, likely due to pleiotropic effects and linkages between the two colocalized systems. Plasticity continues to evolve within the urchins with numerous instances of losses associated with loss of sensory capabilities and in one case loss of neurons, consistent with a cost associated with maintaining these capabilities. Thus, evidence was found for the neurosensory system providing opportunities and constraints to the evolution of phenotypic plasticity.

Deciphering Codon Usage Patterns in Genome of Cucumis sativus in Comparison with Nine Species of Cucurbitaceae

Cucumber is the most important vegetable crop in the Cucurbitaceae family. Condon usage bias (CUB) is a valuable character of species evolution. However, there is little research on the CUB of cucumber. Thus, this study analyzes the codon usage patterns of cucumber and its relatives within Cucurbitaceae on the genomic level. The analysis of fundamental indicators of codon characteristics shows that it was slightly GC poor, and there was weak codon usage bias in cucumber. We conduct the analysis of neutrality plot, ENC plot, P2 index, and COA indicates that the nucleotide composition, mutation pressure, and translational selection might play roles in CUB in cucumber and its relatives. Among these factors, nucleotide composition might play the most critical role. Based on these analyses, 30 optimal codons were identified in cucumber, most of them ending with U or A. Meanwhile, based on the RSCU values of species, a cluster tree was constructed, in which the situation of cucumber is consistent with the current taxonomic and evolutionary studies in Cucurbitaceae. This study systematically compared the CUB patterns and shaping factors of cucumber and its relatives, laying a foundation for future research on genetic engineering and evolutionary mechanisms in Cucurbitaceae.

Colonized Niche, Evolution and Function Signatures of Bifidobacterium pseudolongum within Bifidobacterial Genus

Background: Although genomic features of various bifidobacterial species have received much attention in the past decade, information on Bifidobacterium pseudolongum was limited. In this study, we retrieved 887 publicly available genomes of bifidobacterial species, and tried to elucidate phylogenetic and potential functional roles of B. pseudolongum within the Bifidobacterium genus. Results: The results indicated that B. pseudolongum formed a population structure with multiple monophyletic clades, and had established associations with different types of mammals. The abundance of B. pseudolongum was inversely correlated with that of the harmful gut bacterial taxa. We also found that B. pseudolongum showed a strictly host-adapted lifestyle with a relatively smaller genome size, and higher intra-species genetic diversity in comparison with the other tested bifidobacterial species. For functional aspects, B. pseudolongum showed paucity of specific metabolic functions, and enrichment of specific enzymes degrading complex plant carbohydrates and host glycans. In addition, B. pseudolongum possessed a unique signature of probiotic effector molecules compared with the other tested bifidobacterial species. The investigation on intra-species evolution of B. pseudolongum indicated a clear evolution trajectory in which considerable clade-specific genes, and variation on genomic diversity by clade were observed. Conclusions: These findings provide valuable information for explaining the host adaptability of B. pseudolongum, its evolutionary role, as well as its potential probiotic effects.

Biology before the SOS Response—DNA Damage Mechanisms at Chromosome Fragile Sites

The Escherichia coli SOS response to DNA damage, discovered and conceptualized by Evelyn Witkin and Miroslav Radman, is the prototypic DNA-damage stress response that upregulates proteins of DNA protection and repair, a radical idea when formulated in the late 1960s and early 1970s. SOS-like responses are now described across the tree of life, and similar mechanisms of DNA-damage tolerance and repair underlie the genome instability that drives human cancer and aging. The DNA damage that precedes damage responses constitutes upstream threats to genome integrity and arises mostly from endogenous biology. Radman’s vision and work on SOS, mismatch repair, and their regulation of genome and species evolution, were extrapolated directly from bacteria to humans, at a conceptual level, by Radman, then many others. We follow his lead in exploring bacterial molecular genomic mechanisms to illuminate universal biology, including in human disease, and focus here on some events upstream of SOS: the origins of DNA damage, specifically at chromosome fragile sites, and the engineered proteins that allow us to identify mechanisms. Two fragility mechanisms dominate: one at replication barriers and another associated with the decatenation of sister chromosomes following replication. DNA structures in E. coli, additionally, suggest new interpretations of pathways in cancer evolution, and that Holliday junctions may be universal molecular markers of chromosome fragility.

Zebrafish as a Model for Germ Cell Regeneration

Germ cell acts as a link between transfer of genetic information and process of species evolution. Defects or malformations of germ cells can lead to infertility or tumors. Germ cell regeneration is one of the effective ways to treat the infertility. Therefore, it is of great scientific and clinical interests to dissect the cellular and molecular mechanisms underlying germ cell regeneration. Progress have already been achieved in germ cell regeneration using model organisms for decades. However, key open issues regarding the underpinning mechanisms still remain poorly understood. Zebrafish is well known for its powerful regenerative capacity to regenerate various tissues and organs. Recently, advances in genomics, genetics, microscopy, and single cell technologies have made zebrafish an attractive model to study germ cell development and regeneration. Here we review recent technologies for the study of germ cell regeneration in zebrafish, highlight the potential of germline stem cells (GSCs) in the contribution to reproductive system regeneration, and discuss the nanos. Wnt signaling and germ cell-specific factors involved in the regulation of germ cell regeneration.

Systemic aneuploidization events drive phenotype switching in Saccharomyces cerevisiae

How cells leverage their phenotypic potential to adapt and survive in a changing environment is a complex biological problem, with important implications for pathogenesis and species evolution. One particularly fascinating adaptive approach is the bet hedging strategy known as phenotype switching, which introduces phenotypic variation into a population through stochastic processes. Phenotype switching has long been observed in species across the tree of life, yet the mechanistic causes of switching in these organisms have remained difficult to define. Here we describe the causative basis of colony morphology phenotype switching which occurs among cells of the pathogenic isolate of Saccharomyces cerevisiae, YJM311. From clonal populations of YJM311 cells grown in identical conditions, we identified colonies which displayed altered colony architectures, yet could revert to the wild-type morphology after passaging. Whole genome sequence analysis revealed that these variant clones had all acquired whole chromosome copy number alterations (i.e., aneuploidies). Cumulatively, the variant clones we characterized harbored an exceptional spectrum of karyotypic alterations, with individual variants carrying between 1 and 16 aneuploidies. Most variants harbored unique collections of aneuploidies, indicating that numerous distinct karyotypes could manifest in the same morphological variation. Intriguingly, the genomic stability of these newly aneuploid variant clones modulated how often cells reverted back to the wild-type phenotypic state. We found that such revertant switches were also driven by chromosome missegregation events, and in some cases occurred through a return to euploidy. Together, our results demonstrate that colony morphology switching in this yeast strain is driven by stochastic and systemic aneuploidization events. These findings add an important new perspective to our current understanding of phenotype switching and bet hedging strategies, as well as how environmental pressures perpetuate organismal adaption and genome evolution.