Biology subjects

Nagy, P. L.

Publications and source records attributed to Nagy, P. L..

3 recordsLinked to original sources

bioRxiv2026

Genomic landscape of the medieval Hungarian elite from the Szekesfehervar royal necropolis

We analyzed 399 shotgun genomes from the Royal Basilica of Szekesfehervar, representing the elite of the Medieval Hungarian Kingdom. Our results reveal that the Carpathian Basin population underwent a marked homogenization during the Middle Ages, driven largely by admixture with eastern immigrant groups, especially the conquering Hungarians, resulting in a genomic landscape distinct from that of the surrounding European populations. The European ancestry component also shifted: the Avar-period Balkan element disappeared, while northern and northwestern European ancestry increased, likely reflecting changing political connections. We identified a previously unrecognized Conquest-period stratum at the site, including two individuals closely related to the Arpad dynasty. No large, continuous kinship networks were detected, indicating a dynamic and continuously renewed elite. At the population level, the strongest affinities were observed with the Conq_Asia_Core group and its ancestor, the Karayakupovo horizon, as well as with medieval populations from neighboring regions (present-day Croatia, Serbia, Slovakia, Poland, and Montenegro), reflecting the diverse sources of the medieval Hungarians.

genetics↗

bioRxiv2022

Whole genome analysis sheds light on the genetic origin of Huns, Avars and conquering Hungarians

Huns, Avars and conquering Hungarians were Migration Period nomadic groups which arrived in three successive waves in the Carpathian Basin between the 5th and 9th centuries. Based on historical data each of these groups are thought to have arrived from Asia, although their exact origin and relation to other ancient and modern populations has been debated. In this study we have sequenced 9 Hun, 143 Avar and 113 Hungarian conquest period samples, and identified three core populations, representing immigrants from each period, with no recent European ancestry. Our results suggest that this "immigrant core" of both Huns and Avars originated in present day Mongolia, and their origin can be traced back to Xiongnus. On the other hand, the "immigrant core" of the conquering Hungarians derived from an earlier admixture of Mansis, early Sarmatians and descendants of late Xiongnus. In addition, we detected shared Hun-related ancestry in numerous Avar and Hungarian conquest period genetic outliers indicating a genetic link between these successive nomadic groups. Aside from the immigrant core groups we identified that the majority of the individuals from each period were local residents, harboring "native European" ancestry.

genetics↗

bioRxiv2019

Allele-specific DNA methylation is increased in cancers and its dense mapping in normal plus neoplastic cells increases the yield of disease-associated regulatory SNPs

BackgroundMapping of allele-specific DNA methylation (ASM) can be a post-GWAS strategy for localizing regulatory sequence polymorphisms (rSNPs). However, the advantages of this approach, and the mechanisms underlying ASM in normal and neoplastic cells, remain to be clarified. ResultsWe performed whole genome methyl-seq on diverse normal cells and tissues and three types of cancers (multiple myeloma, lymphoma, glioblastoma multiforme). After excluding imprinting, the data pinpointed 15,114 high-confidence ASM differentially methylated regions (DMRs), of which 1,842 contained SNPs in strong linkage disequilibrium or coinciding with GWAS peaks. ASM frequencies were increased 5 to 9-fold in cancers vs. matched normal tissues, due to widespread allele-specific hypomethylation and focal allele-specific hypermethylation in poised chromatin. Cancers showed increased allele switching at ASM loci, but disruptive SNPs in specific classes of CTCF and transcription factor (TF) binding motifs were similarly correlated with ASM in cancer and non-cancer. Rare somatic mutations affecting these same motif classes tracked with de novo ASM in the cancers. Allele-specific TF binding from ChIP-seq was enriched among ASM loci, but most ASM DMRs lacked such annotations, and some were found in otherwise uninformative "chromatin deserts". ConclusionsASM is increased in cancers but occurs by a shared mechanism involving disruptive SNPs in CTCF and TF binding sites in both normal and neoplastic cells. Dense ASM mapping in normal plus cancer samples reveals candidate rSNPs that are difficult to find by other approaches. Together with GWAS data, these rSNPs can nominate specific transcriptional pathways in susceptibility to autoimmune, neuropsychiatric, and neoplastic diseases. Custom genome browser tracks with annotated ASM loci can be viewed at a UCSC browser session hosted by our laboratory (https://bit.ly/tycko-asm)

genomics↗