Gene Literature Dashboard

<h4>Background</h4>Transitioning from pediatric to adult HIV care is critical for adolescents and young adults living with HIV (AYLH). This study assessed the timing and factors associated with this transition in Asia.<h4>Setting</h4>Retrospective study of AYLH enrolled in Therapeutics Research, Education, and AIDS Training Asia Pediatric HIV Observational Database clinics between May 1991 and December 2020.<h4>Methods</h4>Eligible AYLH were categorized into <18-year-old transitions, and ≥18-year-old transitions or continued pediatric care.<h4>Results</h4>The analysis included 1803 AYLH from 6 countries. Of these, 92.7% (n = 1672) had perinatally acquired HIV, and 69.9% (n = 1260) were ≥18-year-old transitions or continued pediatric care. Excluding AYLH who remained in pediatric care, median age at transition was 16.1 years (interquartile range [IQR]: 14.9-17.0) for <18-year-old transitions and 20.0 years (IQR: 19.1-21.2) for ≥18-year-old transitions. At age 18, among 1368 AYLH with available viral load data, 72.9% (n = 998) had viral loads <50 copies/mL (78.9% in <18-year-old transitions [n = 310/393] vs 70.6% in ≥18-year-old transitions [n = 688/975]; P = 0.002). The median CD4 count was 635 cells/μL (IQR: 450-842). Factors independently associated with transitions at ≥18-year-old or continued pediatric care included residence in an upper-middle-income country (adjusted odds ratio [aOR] 10.68 [95% confidence interval (CI): 7.76 to 14.68], P < 0.001), living with family (aOR 2.81 [95% CI: 1.99 to 3.97], P < 0.001), and previous antiretroviral therapy class switching (aOR 1.91 [95% CI: 1.34 to 2.72], P < 0.001).<h4>Conclusion</h4>Most AYLH in this cohort transitioned at ≥18 years of age. About one-fourth had unsuppressed viral loads at age 18, irrespective of transition status, underscoring the need for personalized treatment approaches that support antiretroviral therapy adherence from pediatric care, preparing AYLH for transition to adult clinics.

Myelinogenesis is insufficient in numerous myelin-related diseases in the CNS, leading to functional impairments. Myelinogenesis couples with angiogenesis to ensure adequate need of oxygen and nutrients for oligodendrocyte (OL) differentiation. However, approaches to synchronize myelino-vascular coupling remain unavailable. We hypothesize the identification of shared signaling pathways in vascular cells and oligodendroglia may yield novel strategies to promote myelin repair through strengthening the blood vessel-myelination coupling. Here, single-cell sequencing and in situ hybridization revealed high expression of G-protein-coupled receptor 30 (Gpr30) in both vascular cells and oligodendroglia, with selective enrichment in pericytes and oligodendrocyte precursor cells (OPCs). Cell-specific deletion of GPR30 in pericytes driven by PDGFRβ^CreERT2 resulted in enhanced angiogenesis and myelination in developing brains. GPR30 deletion in OPCs or antagonizing GPR30 by G15 resulted in increased MBP-positive cell density and enhanced nanofiber wrapping capacity in vitro, thereby demonstrating an inhibiting role of GPR30 on OPC differentiation. To elucidate the coordinative role of GPR30 in both cell types, we employed NG2^CreERT to induce a conditional knockout of GPR30 in both NG2-positive pericytes and OPCs. The conditional deletion of GPR30 enhanced myelination and increased vascular density in developing brains. Further, GPR30 cKO or G15 treatment enhanced myelin repair and functional recovery in the chronic neonatal hypoxia and lysolecithin-induced demyelination model, suggesting that antagonizing GPR30 is a promising strategy to synchronize angiogenesis with myelination to promote myelinogenesis. These findings establish GPR30 antagonism as a promising approach to enhance myelin repair through synchronizing pericyte-mediated angiogenesis and OPC differentiation.

Glial cells, including radial glia, oligodendrocyte precursor cells (OPCs), oligodendrocytes, astrocytes, and microglia, are active and dynamic regulators of central nervous system (CNS) development, homeostasis, and disease. Through extensive interactions with neurons, other glial populations, and the vasculature, they form highly specialized communication networks that are essential for normal brain function. While transcriptomic approaches have revealed extensive glial heterogeneity and enabled the prediction of putative signaling networks, a critical challenge remains in validating and translating these findings at the level of distinct protein complexes existing both within and between the various glial cell types. This is largely due to the fact that traditional proteomic technologies lack spatial resolution and/or fail to capture protein interaction networks. Proximity labeling (PL) has emerged as a powerful strategy to overcome these limitations by enabling cell-type-specific mapping of protein networks and subcellular proteomes, with spatial and temporal precision. Emerging studies have applied PL enzymes, such as BioID, TurboID, and HRP, across diverse glial populations, starting to uncover protein networks supporting their interactions with neurons and vascular elements, allowing metabolic support, maintenance of microenvironment homeostasis and cell-cell communication (including synaptic modulation). In this review, we summarize the main PL enzymes, discuss key studies across different glial cell types, and examine the technical challenges and future perspectives of applying PL to investigate glial biology. By complementing transcriptomic data with spatially resolved proteomic insights, PL provides a unique opportunity to deepen our understanding of glial cell biology in health and disease.

The Min pig, a representative northern Chinese indigenous breed, carries a unique ancestral background shaped by the historical phylogeography of Northeast Asia. This study aimed to dissect the population structure, temporal genetic divergence, and ancestral composition of Min pigs, trace their evolutionary origin, and identify trait-linked functional genes, providing information regarding their evolutionary history and conservation. We analyzed 61 Min pigs sampled across nearly 20 years and 701 reference pigs comprising other Chinese indigenous breeds, Western commercial lines, and Chinese wild boars, using PCA, NJ phylogenetic analysis, Admixture, TreeMix, D-statistic, f4-ratio, and combined selection signature scans (sliding-window F_ST, XP-EHH, and π-ratio). Clear genetic stratification was observed among Min pig subpopulations, reflecting long-term divergence under natural and artificial selection. PCA and Admixture (K = 2-4) separated East Asian indigenous and Western ancestral components, verifying an admixed Northeast Asian origin with a dominant ancient East Asian component and a Western component. Compared with early-2000s Min pigs, contemporary individuals are genetically closer to Western breeds and exhibit a more scattered structure due to shifted ancestral component proportions, further confirmed by D-statistic and f4-ratio values. We identified 321 differentiated SNP loci based on the Animal QTL database, corresponding to core candidate genes (AKT3, ACACA, MAP3K5, FGFR4, C3, and SERPINC1) enriched for meat quality, growth, reproduction, immunity, energy metabolism, and MAPK/PI3K-Akt/AMPK pathways. This study reveals Min pigs' admixed origin and temporal divergence, clarifying their Northeast Asian evolution and providing molecular markers for genetic monitoring and conservation.

Wattles are finger-like appendages on the ventral neck of goats, serving as a distinctive morphological marker for breed identification that serves potential implications for production performance. However, their genetic basis remains incompletely characterized. Here, we integrated a genome-wide association study (GWAS) and selection signature analysis to identify candidate genes and genomic regions associated with the wattle trait in goats. Using a linear mixed model, GWAS on 463 goats (23 wattled and 440 non-wattled) identified 385 quantitative trait loci (QTLs) at a 5% false discovery rate, yielding 346 candidate genes. The most significant association signal was observed on chromosome 10 (72.61-73.48 Mb), where the lead SNP (rs636481767) is located within a region containing GJD2, GREM1, and FMN1, showing strong linkage disequilibrium (r² > 0.6) with surrounding loci. Subsequent selection signature analysis (23 wattled and 23 non-wattled) identified 83 genomic regions harboring 119 candidate genes. The strongest signals were detected at MFSD14B on chromosome 8 (F_ST = 0.154, log₂π-ratio = 2.611) and PDLIM7 on chromosome 7 (F_ST = 0.144, log₂π-ratio = 0.806). KEGG pathway enrichment analysis revealed that GWAS-associated genes were involved in glycosylation and immune responses, whereas selection-signature genes were enriched in DNA repair and the Hippo, Notch, and Wnt pathways. Furthermore, cross-species PheWAS revealed that human FMN1 is associated with dermatological, skeletal, and metabolic phenotypes, while porcine FMN1 is associated with backfat thickness and loin muscle depth. Overall, this study provides molecular markers of potential value for goat breeding and pinpoints key candidate genes for future functional validation of wattle development.