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Pre-mRNA splicing is the process by which introns are removed and the protein coding elements assembled into mature mRNAs. Alternative pre-mRNA splicing provides an important source of transcriptome and proteome complexity through selectively joining different coding elements to form mRNAs, which encode proteins with similar or distinct functions. In mammals, previous studies have shown the role of alternative splicing in regulating the function of the immune system, especially in the regulation of T-cell activation and function. As lower vertebrates, teleost fish mainly rely on a large family of pattern recognition receptors (PRRs) to recognize pathogen-associated molecular patterns (PAMPs) from various invading pathogens. In this review, we summarize recent advances in our understanding of alternative splicing of piscine PRRs including peptidoglycan recognition proteins (PGRPs), nucleotide binding and oligomerization domain (NOD)-like receptors (NLRs), retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs) and their downstream signaling molecules, compared to splicing in mammals. We also discuss what is known and unknown about the function of splicing isoforms in the innate immune responses against pathogens infection in mammals and teleost fish. Finally, we highlight the consequences of alternative splicing in the innate immune system and give our view of important directions for future studies. [ABSTRACT FROM AUTHOR]

In fast-varying channels, an orthogonal frequency-division multiplexing system needs to insert denser pilot symbols among transmitted symbols in tracking the variation of a channel. However, using denser pilot symbols reduces transmission throughput. In this paper, we propose a pseudopilot algorithm for data detection in fast-varying channels without increasing the pilot density. Our algorithm is based on a regressional model-based least-squares-fitting approach. Within a block of received symbols, we select some data symbols and regard them as pseudopilot symbols. The receiver considers all the possible patterns of the pseudopilots and associates each of them with a data sequence and a corresponding metric. The associated data sequence, whose metric is minimum, is selected as the detected data sequence. Our algorithm is not based on a decision-directed or decision-feedback architecture because the pseudopilots do not come from any detected symbols. The proposed algorithm needs to search all the possible patterns of the pseudopilots, and the complexity may increase with the number of pseudopilots and constellation size. To reduce the number of search, we further propose two modified approaches. The simulation results show that the performance of the proposed algorithms could approach a bit-error probability lower bound that is obtained by letting the receiver know the true values of the pseudopilots. Compared with the linear interpolation method, the proposed algorithm shows obvious improvement in fast-varying channels. The proposed modified approaches could also effectively reduce the number of search while maintaining the performance. We also give the complexity analysis of the proposed algorithm and an approach to determine the degree of the regression polynomial. [ABSTRACT FROM AUTHOR]

This paper considers the problem of blind, joint channel estimation and data detection for orthogonal frequency-division multiplexing (OFDM) systems in a fading environment. Employing a regression model for a time-varying channel, we convert the problem into one that finds the data sequence x whose associated least-squares (LS) channel estimate z(x) is closest to the space of some regression curves (surfaces). We apply the branch-and-bound principle to solve the nonlinear integer programming problem associated with finding the curve that fits a subchannel in the LS sense. A recursive formula for fast metric update is obtained by exploiting the intrinsic characteristic of our objective function. The impacts of reordering the data sequence and selective detection are addressed. By employing a preferred order along with a selective detection method, we greatly reduce the detector complexity while giving up little performance loss. Both the complete and the reduced-complexity algorithms can be used for blind and semiblind detections of OFDM signals in a subchannel-by-subchannel manner. To further reduce the complexity and exploit the frequency-domain channel correlation, we suggest a two-stage approach that detects a few selected positions in some subchannels first, and then, treating the detected symbols as pilots, determines the remaining symbols within a properly chosen time-frequency block by a two-dimensional model-based pilot-assisted algorithm. The proposed methods do not require the information of the channel statistics like signal-to-noise ratio or channel correlation function. Performance of differential modulations like differential quaternary phase-shift keying and STAR 16-ary quadrature amplitude modulation are provided. Both blind and semiblind schemes yield satisfactory performance. [ABSTRACT FROM AUTHOR]

Focuses on a study which proposed the pilot-assisted channel estimation method for orthogonal frequency division multiplexing signals. Discussion on the Rayleigh fading effect; Application of linear mean-squared error in channel estimation; Sample computation of signal-to-noise ratio; Methodology and results.

Tripartite motif (TRIM) proteins are involved in different cellular functions, including regulating virus infection. In teleosts, two orthologous genes of mammalian TRIM2 are identified. However, the functions and molecular mechanisms of piscine TRIM2 remain unclear. Here, we show that trim2b-knockout zebrafish are more susceptible to spring viremia of carp virus (SVCV) infection than wild-type zebrafish. Transcriptomic analysis demonstrates that NOD-like receptor (NLR), but not RIG-I-like receptor (RLR), signaling pathway is significantly enriched in the trim2b-knockout zebrafish. In vitro, overexpression of Trim2b fails to degrade RLRs and those key proteins involved in the RLR signaling pathway but does for negative regulators NLRP12-like proteins. Zebrafish Trim2b degrades NLRP12-like proteins through its NHL_TRIM2_like and IG_FLMN domains in a ubiquitin-proteasome degradation pathway. SVCV-N and SVCV-G proteins are also degraded by NHL_TRIM2_like domains, and the degradation pathway is an autophagy lysosomal pathway. Moreover, zebrafish Trim2b can interfere with the binding between NLRP12-like protein and SVCV viral RNA and can completely block the negative regulation of NLRP12-like protein on SVCV infection. Taken together, our data demonstrate that the mechanism of action of zebrafish trim2b against SVCV infection is through targeting the degradation of host-negative regulators NLRP12-like receptors and viral SVCV-N/SVCV-G genes. IMPORTANCE Spring viremia of carp virus (SVCV) is a lethal freshwater pathogen that causes high mortality in cyprinid fish. In the present study, we identified zebrafish trim2b, NLRP12-L1, and NLRP12-L2 as potential pattern recognition receptors (PRRs) for sensing and binding viral RNA. Zebrafish trim2b functions as a positive regulator; however, NLRP12-L1 and NLRP12-L2 function as negative regulators during SVCV infection. Furthermore, we find that zebrafish trim2b decreases host lethality in two manners. First, zebrafish Trim2b promotes protein degradations of negative regulators NLRP12-L1 and NLRP12-L2 by enhancing K48-linked ubiquitination and decreasing K63-linked ubiquitination. Second, zebrafish trim2b targets viral RNAs for degradation. Therefore, this study reveals a special antiviral mechanism in lower vertebrates. [ABSTRACT FROM AUTHOR]

Nucleotide oligomerization domain-like receptors (NLRs) and RIG-I-like receptors (RLRs) detect diverse pathogen-associated molecular patterns to activate the innate immune response. The role of mammalian NLR NOD1 in sensing bacteria is well established. Although several studies suggest NOD1 also plays a role in sensing viruses, the mechanisms behind this are still largely unknown. In this study, we report on the synergism and antagonism between NOD1 and MDA5 isoforms in teleost. In zebrafish, the overexpression of NOD1 enhances the antiviral response and mRNA abundances of key antiviral genes involved in RLR-mediated signaling, whereas the loss of NOD1 has the opposite effect. Notably, spring viremia of carp virus-infected NOD1-/- zebrafish exhibit reduced survival compared with wild-type counterparts. Mechanistically, NOD1 targets MDA5 isoforms and TRAF3 to modulate the formation of MDA5-MAVS and TRAF3-MAVS complexes. The cumulative effects of NOD1 and MDA5a (MDA5 normal form) were observed for the binding with poly(I:C) and the formation of the MDA5a-MAVS complex, which led to increased transcription of type I IFNs and ISGs. However, the antagonism between NOD1 and MDA5b (MDA5 truncated form) was clearly observed during proteasomal degradation of NOD1 by MDA5b. In humans, the interactions between NOD1-MDA5 and NOD1-TRAF3 were confirmed. Furthermore, the roles that NOD1 plays in enhancing the binding of MDA5 to MAVS and poly(I:C) are also evolutionarily conserved across species. Taken together, our findings suggest that mutual regulation between NOD1 and MDA5 isoforms may play a crucial role in the innate immune response and that NOD1 acts as a positive regulator of MDA5/MAVS normal form-mediated immune signaling in vertebrates. [ABSTRACT FROM AUTHOR]