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Hadal environments (depths below 6,000 m) are characterized by extremely high hydrostatic pressures, low temperatures, a scarce food supply, and little light. The evolutionary adaptations that allow vertebrates to survive in this extreme environment are poorly understood. Here, we constructed a high-quality reference genome for Yap hadal snailfish (YHS), which was captured at a depth of ~7,000 m in the Yap Trench. The final YHS genome assembly was 731.75 Mb, with a contig N50 of 0.75 Mb and a scaffold N50 of 1.26 Mb. We predicted 24,329 protein-coding genes in the YHS genome, and 24,265 of these genes were successfully functionally annotated. Phylogenetic analyses suggested that YHS diverged from a Mariana Trench snailfish approximately 0.92 million years ago. Many genes associated with DNA repair show evidence of positive selection and have expanded copy numbers in the YHS genome, possibly helping to maintain the integrity of DNA under increased hydrostatic pressure. The levels of trimethylamine N-oxide (TMAO), a potent protein stabilizer, are much higher in the muscles of YHS than in those of shallow-water fish. This difference is perhaps due to the five copies of the TMAO-generating enzyme flavin-containing monooxygenase-3 gene (fmo3) in the YHS genome and the abundance of trimethylamine (TMA)-generating bacteria in the YHS gut. Thus, the high TMAO content might help YHS adapt to high hydrostatic pressure by improving protein stability. Additionally, the evolutionary features of the YHS genes encoding sensory-related proteins are consistent with the scarce food supply and darkness in the hadal environments. These results clarify the molecular mechanisms underlying the adaptation of hadal organisms to the deep-sea environment and provide valuable genomic resources for in-depth investigations of hadal biology. Author summary: Hadal environments (depths below 6,000 m) are characterized by extremely high hydrostatic pressures, low temperatures, a scarce food supply, and little light. Fish are the only vertebrates inhabiting the hadal zone, and hadal snailfishes have been found in at least five geographically separated marine trenches. However, the genetic mechanisms that allow vertebrates to live in such extreme conditions are not well understood. Here, we constructed a high-quality reference genome for Yap hadal snailfish (YHS) captured at a depth of ~7,000 m in the Yap Trench, using long reads obtained by Pacific Biosciences Sequel sequencing. Comparative genomic analyses revealed that many genes associated with DNA repair show evidence of positive selection and have expanded copy numbers in the YHS genome, which potentially reflect the difficulty of maintaining DNA integrity under high hydrostatic pressure. Moreover, the five copies of the trimethylamine N-oxide (TMAO)-generating enzyme flavin-containing monooxygenase-3 gene (fmo3) and the abundance of trimethylamine (TMA)-generating bacteria in the YHS gut could provide enough TMAO to improve protein stability under hadal conditions. In addition, characteristics of the YHS sensory system genes were consistent with the scarce food supply and darkness in the hadal zone. Our results provide new insights into the molecular mechanisms underlying the adaptation of hadal organisms to the deep-sea environment and valuable genomic resources that will help further clarify hadal adaptations. [ABSTRACT FROM AUTHOR]

Stomata are specialized pores in the epidermis of the aerial parts of a plant, where stomatal guard cells close and open to regulate gas exchange with the atmosphere and restrict excessive water vapor from the plant. The production and patterning of the stomatal lineage cells in higher plants are influenced by the activities of the widely-used mitogen-activated protein kinase (MAPK) signaling components. The phenotype caused by the loss-of-function mutations suggested pivotal roles of the canonical MAPK pathway in the suppression of stomatal formation and regulation of stomatal patterning in Arabidopsis, whilst the cell type-specific manipulation of individual MAPK components revealed the existence of a positive impact on stomatal production. Among a large number of putative MAPK substrates in plants, the nuclear transcription factors SPEECHLESS (SPCH) and SCREAM (SCRM) are targets of MAPK 3 and 6 (MPK3/6) in the inhibition of stomatal formation. The polarity protein BREAKING OF ASYMMETRY IN THE STOMATAL LINEAGE (BASL) is phosphorylated by MPK3/6 for localization and function in driving divisional asymmetries. Here, by functionally characterizing three MAPK SUBSTRATES IN THE STOMATAL LINEAGE (MASS) proteins, we establish that they are plasma membrane-associated, positive regulators of stomatal production. MPK6 can phosphorylate the MASS proteins in vitro and mutating the putative substrate sites interferes the subcellular partition and function of MASS in planta. Our fine-scale domain analyses identify critical subdomains of MASS2 required for specific subcellular localization and biological function, respectively. Furthermore, our data indicate that the MASS proteins may directly interact with the MAPKK Kinase YODA (YDA) at the plasma membrane. Thus, the deeply conserved MASS proteins are tightly connected with MAPK signaling in Arabidopsis to fine-tune stomatal production and patterning, providing a functional divergence of the YDA-MPK3/6 cascade in the regulation of plant developmental processes. Author summary: Stomata surrounded by guard cells are breathing pores in the plant epidermis, where they open to allow gas exchange and close to restrict water loss. The production and patterning of stomata in the model plant Arabidopsis provide an ideal genetic and cell biological system for studying the molecular mechanisms underlying developmental program and plasticity in responding to environmental changes. The MAPK cascades are ubiquitous signaling modules in eukaryotes. They regulate diverse cellular programs by relaying extracellular signals to intracellular regulators. In the model plant Arabidopsis, MAPK 3 and 6 were found to phosphorylate several protein substrates in the nucleus and cytoplasm to regulate stomatal development and patterning. In this study, we report that a group of new MAPK substrates, the MASS proteins, function at the plasma membrane to regulate stomatal production and patterning in Arabidopsis. Thus, the output of MAPK signaling in the regulation of stomatal development is diverged by differentially localized substrates, suggesting that the concerted activities of MAPK substrates fine-tune stomatal development to ultimately improve plant adaptability to the changing environment. [ABSTRACT FROM AUTHOR]

Background: Schistosomiasis japonica has been resurging in certain areas of China where its transmission was previously well controlled or interrupted. Several factors may be contributing to this, including mobile populations, which if infected, may spread the disease. A wide range of estimates have been published for S. japonicum infections in mobile populations, and a synthesis of these data will elucidate the relative risk presented from these groups. Methods: A literature search for publications up to Oct 31, 2014 on S. japonicum infection in mobile populations in previously endemic but now non-endemic regions was conducted using four bibliographic databases: China National Knowledge Infrastructure, WanFang, VIP Chinese Journal Databases, and PubMed. A meta-analysis was conducted by pooling one arm binary data with MetaAnalyst Beta 3.13. The protocol is available on PROSPERO (No. CRD42013005967). Results: A total of 41 studies in Chinese met the inclusion criteria, covering seven provinces of China. The time of post-interruption surveillance ranged from the first year to the 31st year. After employing a random-effects model, from 1992 to 2013 the pooled seroprevalence ranged from 0.9% (95% CI: 0.5-1.6%) in 2003 to 2.3% (95% CI: 1.5-3.4) in 1995; from the first year after the disease had been interrupted to the 31st year, the pooled seroprevalence ranged from 0.6% (95% CI: 0.2-2.1%) in the 27th year to 4.0% (95%CI: 1.3-11.3%) in the second year. The pooled seroprevalence in mobile populations each year was significantly lower than among the residents of endemic regions, whilst four papers reported a lower level of infection in the mobile populations than in the local residents out of only 13 papers which included this data. Conclusions: The re-emergence of S. japonicum in areas which had previously interrupted transmission might be due to other factors, although risk from re-introduction from mobile populations could not be excluded. [ABSTRACT FROM AUTHOR]

The long-term potentiation (LTP) of spinal C-fiber-evoked field potentials is considered as a fundamental mechanism of central sensitization in the spinal cord. Accumulating evidence has showed the contribution of spinal microglia to spinal LTP and pathological pain. As a key signaling of neurons-microglia interactions, the involvement of CX3CL1/CX3CR1 signaling in pathological pain has also been investigated extensively. The present study examined whether CX3CL1/CX3CR1 signaling plays a role in spinal LTP. The results showed that 10-trains tetanic stimulation (100 Hz, 2s) of the sciatic nerve (TSS) produced a significant LTP of C-fiber-evoked field potentials lasting for over 3 h in the rat spinal dorsal horn. Blockade of CX3CL1/CX3CR1 signaling with an anti-CX3CR1 neutralizing antibody (CX3CR1 AB) markedly suppressed TSS-induced LTP. Exogenous CX3CL1 significantly potentiated 3-trains TSS-induced LTP in rats. Consistently, spinal LTP of C-fiber-evoked field potentials was also induced by TSS (100 Hz, 1s, 4 trains) in all C57BL/6 wild type (WT) mice. However, in CX3CR1-/- mice, TSS failed to induce LTP and behavioral hypersensitivity, confirming an essential role of CX3CR1 in spinal LTP induction. Furthermore, blockade of IL-18 or IL-23, the potential downstream factors of CX3CL1/CX3CR1 signaling, with IL-18 BP or anti-IL-23 neutralizing antibody (IL-23 AB), obviously suppressed spinal LTP in rats. These results suggest that CX3CL1/CX3CR1 signaling is involved in LTP of C-fiber-evoked field potentials in the rodent spinal dorsal horn. [ABSTRACT FROM AUTHOR]