Integrative genomic phylogeography reveals signs of mitonuclear incompatibility in a natural hybrid goby population

Hybridization between divergent lineages generates new allelic combinations. One mechanism that can hinder the formation of hybrid populations is mitonuclear incompatibility, that is, dysfunctional interactions between proteins encoded in the nuclear and mitochondrial genomes (mitogenomes) of diverged lineages. Theoretically, selective pressure due to mitonuclear incompatibility can affect genotypes in a hybrid population in which nuclear genomes and mitogenomes from divergent lineages admix. To directly and thoroughly observe this key process, we de novo sequenced the 747‐Mb genome of the coastal goby, Chaenogobius annularis, and investigated its integrative genomic phylogeographics using RNA‐sequencing, RAD‐sequencing, genome resequencing, whole mitogenome sequencing, amplicon sequencing, and small RNA‐sequencing. Chaenogobius annularis populations have been geographically separated into Pacific Ocean (PO) and Sea of Japan (SJ) lineages by past isolation events around the Japanese archipelago. Despite the divergence history and potential mitonuclear incompatibility between these lineages, the mitogenomes of the PO and SJ lineages have coexisted for generations in a hybrid population on the Sanriku Coast. Our analyses revealed accumulation of nonsynonymous substitutions in the PO‐lineage mitogenomes, including two convergent substitutions, as well as signals of mitochondrial lineage‐specific selection on mitochondria‐related nuclear genes. Finally, our data implied that a microRNA gene was involved in resolving mitonuclear incompatibility. Our integrative genomic phylogeographic approach revealed that mitonuclear incompatibility can affect genome evolution in a natural hybrid population.     

Co‐suppression in Pyropia yezoensis (Rhodophyta) Reveals the Role of PyLHCI in Light Harvesting and Generation Switch

The red macroalga Pyropia yezoensis is an economically important seaweed widely cultured in Asian countries and is a model organism for molecular biological and commercial research. This species is unique in that it utilizes both phycobilisomes and transmembrane light‐harvesting proteins as its antenna system. Here, one of the genes of P. yezoensis (PyLHCI) was selected for introduction into its genome to overexpress PyLHCI. However, the co‐suppression phenomenon occurred. This is the first documentation of co‐suppression in algae, in which it exhibits a different mechanism from that in higher plants. The transformant (T1) was demonstrated to have higher phycobilisomes and lower LHC binding pigments, resulting in a redder color, higher sensitivity to salt stress, smaller in size, and slower growth rate than the wildtype (WT). The photosynthetic performances of T1 and WT showed similar characteristics; however, P700 reduction was slower in T1. Most importantly, T1 could release a high percentage of carpospores in young blades to switch generation during its life cycle, which was rarely seen in WT. The co‐suppression of PyLHCI revealed its key roles in light harvesting, stress resistance, and generation alternation (generation switch from gametophytes to sporophytes, and reproduction from asexual to sexual).     

Linking Physiology To Ecological Function: Environmental Conditions Affect Performance And Size Of The Intertidal Kelp Hedophyllum Sessile (Laminariales,Phaeophyceae)

For autogenic ecosystem engineers, body size is an aspect of individual performance that has direct connections to community structure; yet the complex morphology of these species can make it difficult to draw clear connections between the environment and performance. We combined laboratory experiments and field surveys to test the hypothesis that individual body size was determined by disparate localized physiological responses to environmental conditions across the complex thallus of the intertidal kelp Hedophyllum sessile, a canopy‐forming physical ecosystem engineer. We documented substantial (> 40%) declines in whole‐thallus photosynthetic potential (as Maximum Quantum Yield, MQY) as a consequence of emersion, which were related to greater than 10‐fold increases in intra‐thallus MQY variability (as Coefficient of Variation). In laboratory experiments, desiccation and high light levels during emersion led to lasting impairment of photosynthetic potential and an immediate > 25% reduction in area due to tissue contraction, which was followed by complete loss of structural integrity after three days of submersion. Tissue exposed to desiccation and high light during emersion had higher nitrogen concentrations and lower phlorotannin concentrations than tissue in control treatments (on average 1.36 and 0.1x controls, respectively), suggesting that conditions during emersion have the potential to affect food quality for consumers. Our data indicate that the complex thallus morphology of H. sessile may be critical to this kelp’s ability to persist in the intertidal zone despite the physiological challenges of emersion and encourage a more nuanced view of the concept of “sub‐lethal stress” on the scale of the whole individual.     

Incorporation of the Tat cell‐penetrating peptide into nanofibers improves the respective antitumor immune response

A major challenge for the development of anticancer vaccines is the induction of a safe and effective immune response, particularly mediated by CD8+ T lymphocytes, in an adjuvant‐free manner. In this respect, we present a simple strategy to improve the specific CD8+ T cell responses using KFE8 nanofibers bearing a Class I (Kb)‐restricted peptide epitope (called E. nanofibers) without the use of adjuvant. We demonstrate that incorporation of Tat, a cell‐penetrating peptide (CPP) of the HIV transactivator protein, into E. nanofibers remarkably enhanced tumor‐specific CD8+ T cell responses. E. nanofibers containing 12.5% Tat peptide (E.Tat_12.5 nanofiber) increased antigen cross‐presentation by bone marrow‐derived dendritic cells as compared with E. nanofibers, or E. nanofibers containing 25 or 50% the Tat peptide. Uptake of KFE8.Tat_12.5 nanofibers by dendritic cells (DCs) was significantly increased compared with KFE8 nanofiber lacking Tat. Peritoneal and lymph node DCs of mice immunized with E.Tat_12.5 nanofibers exhibited increased presentation of the H2kb‐epitope (reminiscent for cross‐presentation) compared with DCs obtained from E. nanofiber vaccinated mice. Tetrameric and intracellular cytokine staining revealed that vaccination with E.Tat_12.5 triggered a robust and specific CD8+ T lymphocyte response, which was more pronounced than in mice vaccinated with E. nanofibers alone. Furthermore, E.Tat_12.5 nanofibers were more potent than E. nanofiber to induce antitumor immune response and tumor‐infiltrating IFN‐γ CD8 T lymphocyte. In terms of cancer vaccine development, we propose that harnessing the nanofiber‐based vaccine platform with incorporated Tat peptide could present a simple and promising strategy to induce highly effective antitumor immune response.     

FGF21 impedes peripheral myelin development by stimulating p38 MAPK/c‐Jun axis

Fibroblast growth factor 21 (FGF21) as a metabolic stress hormone, is mainly secreted by the liver. In addition to its well‐defined roles in energy homeostasis, FGF21 has been shown to promote remyelination after injury in the central nervous system. In the current study, we sought to examine the potential roles of FGF21 in the peripheral nervous system (PNS) myelination. In the PNS myelin development, Fgf21 expression was reversely correlated with myelin gene expression. In cultured primary Schwann cells (SCs), the application of recombinant FGF21 greatly attenuates myelination‐associated gene expression, including Oct6, Krox20, Mbp, Mpz, and Pmp22. Accordingly, the injection of FGF21 into neonatal rats markedly mitigates the myelination in sciatic nerves. On the contrary, the infusion of the anti‐FGF21 antibody accelerates the myelination. Mechanistically, both extracellular signal‐regulated kinase (ERK) and p38 mitogen‐activated protein kinase (MAPK) were stimulated by FGF21 in SCs and sciatic nerves. Following experiments including pharmaceutical intervention and gene manipulation revealed that the p38 MAPK/c‐Jun axis, rather than ERK, is targeted by FGF21 for mediating its repression on myelination in SCs. Taken together, our data provide a new aspect of FGF21 by acting as a negative regulator for the myelin development process in the PNS via activation of p38 MAPK/c‐Jun.