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Biology subjects

Nguyen, S. K.

Publications and source records attributed to Nguyen, S. K..

5 recordsLinked to original sources

High efficiency gene editing and phenotype generation in avian embryos using lipid nanoparticles as a vector delivery platform

Birds are a longstanding developmental biology model because easy access to their fertilized eggs allows for direct observation and experimental manipulation during any stage of embryonic growth prior to hatching. However, functional genetics studies in avian embryos continue to rely primarily on in ovo electroporation and viral transduction, each of which is limited by variable efficiency, procedure-induced embryonic defects, substantial embryo mortality, and ineffective delivery of gene editing reagents such as CRISPR/Cas9. Here we establish lipid nanoparticle (LNP)-mediated delivery as a reproducible alternative for manipulating gene expression in avian embryos with high viability. Using the chicken embryo (Gallus gallus), we targeted migrating cranial NCCs, which contribute extensively to the craniofacial skeleton. We optimized LNP formulation and injection timing and frequency to build a robust and adaptable pipeline that offers efficient delivery of plasmid DNA and RNA cargos. We show that LNP delivery can support the piggyBac transposon system, enabling persistent reporter expression and long-term labeling of cranial NCC derivatives. To test if LNP-mediated delivery of RNA-based CRISPR/Cas9 components can achieve efficient somatic genome editing in ovo, we targeted Runt-related transcription factor 2 (RUNX2), which is required for osteogenesis. Embryos with RUNX2 edits in their cranial NCCs show a severe loss and disruption of craniofacial ossification on the targeted side of their craniofacial skeletons, demonstrating the potential of this approach for rapid functional interrogation of gene function in vivo. We also show that LNPs can mediate transfection in domestic pigeon (Columba livia) and Pekin duck (Anas platyrhynchos) embryos, indicating this method can be deployed across avians as a vector delivery platform for studying development, disease, and evolution.

developmental biology↗

Long-Term Rock Dove (Columba livia) Primordial Germ Cell Culture: A Tool for Avian Conservation

Primordial germ cells (PGCs) are critical tools for genome engineering and conservation in birds. While culture systems for chicken PGCs have been well established for nearly two decades, efforts to propagate PGCs from other avian species have proved exceptionally challenging, limiting the broader application of artificial reproductive technologies in birds. Here we report the first successful derivation and long-term culture of PGCs from the rock dove, or common pigeon (Columba livia). Guided by transcriptomic profiling of PGCs, we developed a species-specific medium that supports PGC maintenance and expansion. We identify insulin signaling as essential for survival and demonstrate that retinoic acid receptor inhibition, while maintaining vitamin A, is necessary for propagation. Supplementation with BMP4, LIF, GDNF, and pleiotrophin further enhances PGC proliferation. Cultured cells express canonical germline markers and migrate to the gonads following injection into both rock dove and chicken embryos, confirming functional competency. These findings establish a platform for germline manipulation and biobanking in Columbidae, broadening the applicability of reproductive technologies to conservation efforts.

cell biology↗

The Dream and MEC NuRD Complexes reinforce SPR-5/MET-2 maternal reprogramming to maintain the germline-soma distinction

The proper coordination of transcription factors, ATP dependent chromatin remodelers and histone modifications is essential for tissue specific gene expression, but how gene expression is regulated at these different levels is not well understood. In C. elegans, H3K4 methylation that is acquired in the germline is reprorgammed at fertilization by the H3K4me1/2 demethlyase SPR-5/LSD1/KDM1A and the H3K9 methyltransferase MET-2/SETDB1/KMT2E. SPR-5/MET-2 maternal reprogramming is required to help establish the germline-soma distinction and prevent developmental delay by preventing inherited H3K4 methylation from inappropriately maintaining germline gene expression in somatic tissues. To determine if the DREAM transcriptional repressor complex and the MEC NuRD ATP dependent nucleosome remodeling and histone deacetylase complex function to reinforce SPR-5/MET-2 maternal reprogamming, we asked if loss of these complexes affects the ectopic germline transcription and developmental delay in spr-5; met-2 double mutants. We find that knocking down the DREAM or MEC NuRD complexes specifically exacerbates the developmental delay and ectopic expression of germline genes in the soma caused by loss of SPR-5 and MET-2. In addition, the DREAM and MEC NuRD complexes bind together at SPR-5/MET-2 reprogramming targets. These data suggest that the transcriptional repression of DREAM and the ATP dependent chromatin remodeling and deactylation activities of the MEC NuRD complex are required somatically to reinforce maternal histone reporgamming by SPR-5/MET-2. Thus, these data provide a novel example of how gene regulation is coordinated at multiple levels to maintain the germline-soma distinction and ensure proper development.

genetics↗

Encephalomyocarditis virus protein 2B* antagonises innate immune signalling by interacting with 14-3-3 protein family members

Encephalomyocarditis virus (EMCV) has for decades served as an important model RNA virus. Although most of the EMCV proteins are obtained via proteolytic cleavage of a long polyprotein, 2B* is expressed from a short overlapping open reading frame via an unusual protein-stimulated temporally dependent ribosomal frameshifting mechanism. The function of 2B* has not yet been characterised, though mutant viruses that are unable to express 2B* have a small plaque phenotype. Here we show that 2B* binds all seven members of the 14-3-3 protein family during virus infection. Binding is dependent on the 2B* C-terminal sequence RRNSS. IFN-{beta} and IL-6 signalling are impeded following overexpression of 2B* but not a truncated version lacking the RRNSS residues, thus suggesting a 14-3-3-dependent role for 2B* in inhibiting MAVS signalling. We also find that this function is distinct from the effect of 2B* on plaque size, as a virus in which 2B* was similarly truncated exhibited near-wildtype plaque size, thus indicating that 2B* also harbours additional functions. This work provides the first identification of a role of 2B* in innate immune antagonism and expands our knowledge of the protein complement of this important model virus. IMPORTANCEEncephalomyocarditis virus (EMCV) infects a range of species, causing economically important reproductive disorders in pigs and encephalitis and myocarditis in rodents. Due to its wide host range, it is an important model pathogen for investigating virus-host interactions. EMCV expresses an accessory protein, 2B*, from an overlapping open reading frame via an unusual ribosomal frameshifting mechanism. Although the frameshifting mechanism has been established, the function of the 2B* protein had not previously been explored. Here, we determined the host proteins to which 2B* binds and found that it specifically binds to the entire 14-3-3 protein family which, among other roles, contribute to the innate immune response to viral infection in mammalian cells. This interaction requires a specific stretch of amino acids at the end of 2B*. By interacting with the 14-3-3 proteins, 2B* blocks immune response activation. Thus, 2B* is a novel antagonist of innate immunity.

microbiology↗

The SARS-CoV-2 protein ORF3c is a mitochondrial modulator of innate immunity

The SARS-CoV-2 genome encodes a multitude of accessory proteins. Using comparative genomic approaches, an additional accessory protein, ORF3c, has been predicted to be encoded within the ORF3a sgmRNA. Expression of ORF3c during infection has been confirmed independently by ribosome profiling. Despite ORF3c also being present in the 2002-2003 SARS-CoV, its function has remained unexplored. Here we show that ORF3c localises to mitochondria during infection, where it inhibits innate immunity by restricting IFN-{beta} production, but not NF-{kappa}B activation or JAK-STAT signalling downstream of type I IFN stimulation. We find that ORF3c acts after stimulation with cytoplasmic RNA helicases RIG-I or MDA5 or adaptor protein MAVS, but not after TRIF, TBK1 or phospho-IRF3 stimulation. ORF3c co-immunoprecipitates with the antiviral proteins MAVS and PGAM5 and induces MAVS cleavage by caspase-3. Together, these data provide insight into an uncharacterised mechanism of innate immune evasion by this important human pathogen.

microbiology↗