Thursday, January 26, 2023

 

New DNA Discoveries For Goldfoot the Lithuanian Descendant

 Nadene Goldfoot                                             

Nadene Goldfoot                      

                    Grandfather, Nathan Abraham Goldfus/foot
           
  Charles (1906) and Moses (1908) (Morris) Goldfoot
          Uncle Charles and son Nathan Bernard Goldfoot 1934

            father, Morris Goldfoot with daughter, me, 1936
           
David, mother, Mildred Goldfoot nee Robinson finally born in 1942
         

David must be a Q3-L275 or (Q3a1) or (Q1b-L275) in his test showing QBZ67; evidently it's all the same.  After the Big Y Test showing something like 111 alleles, he was labeled as QBZ67.  This new label shows the divide of how geneticists see the Q line of Jews as well, evidently.   Before the Big Y test his label was Q Y2200.

This new report is from :   "Phylogeography of human Y-chromosome haplogroup Q3-L275 from an academic/citizen science collaboration" by Rebekah Adele Canada.

The Y-chromosome haplogroup Q has three major branches: Q1, Q2, and Q3. 

Q1 is found in both Asia and the Americas where it accounts for about 90% of indigenous Native American Y-chromosomes; 

Q2 is found in North and Central Asia; but little is known about the third branch, 

Q3, also named Q1b-L275. Here, we combined the efforts of .population geneticists and genetic genealogists to use the potential of full Y-chromosome sequencing for reconstructing haplogroup Q3 phylogeography and suggest possible linkages to events in population history. 

"We analyzed 47 fully sequenced Y-chromosomes and reconstructed the haplogroup Q3 phylogenetic tree in detail. Haplogroup Q3-L275, derived from the oldest known split within Eurasian/American haplogroup Q, most likely occurred in West or Central Asia in the Upper Paleolithic period. During the Mesolithic and Neolithic epochs, Q3 remained a minor component of the West Asian Y-chromosome pool and gave rise to five branches (Q3a to Q3e), which spread "  or 

".occurred in West or Central Asia in the Upper Paleolithic period. During the Mesolithic and Neolithic epochs, Q3 remained a minor component of the West Asian Y-chromosome pool and gave rise to five branches (Q3a to Q3e), which spread across West, Central and parts of South Asia.

 Around 3–4 millennia ago (Bronze Age), the Q3a branch underwent a rapid expansion, splitting into seven branches, some of which entered Europe. 

One of these branches, Q3a1, was acquired by a population ancestral to Ashkenazi Jews and grew within this population during the 1st millennium AD, reaching up to 5% in present day Ashkenazi. 

This study dataset was generated by a massive Y-chromosome genotyping effort in the genetic genealogy community, and phylogeographic patterns were revealed by a collaboration of population geneticists and genetic genealogists. This positive experience of collaboration between academic and citizen science provides a model for further joint projects. Merging data and skills of academic and citizen science promises to combine, respectively, quality and quantity, generalization and specialization, and achieve a well-balanced and careful interpretation of the paternal-side history of human populations. 

Distribution of Q3-L275 To evaluate the Q3 distribution, we analyzed both academic data from indigenous populations and data from genealogical projects. The frequency distribution map based on academic data (Fig. 2a) reveals that haplogroup Q3-L275 is confined to West Asia and neighboring parts of Central and South Asia – mainly Pakistan, West India, and up to 7% in Iran (see also Table 1). The map based on genealogical project data (Fig. 2b) also reveals the presence of haplogroup Q3-L275 in West Asia and neighboring areas, with a maximum frequency in Pakistan, but also throughout Europe. When data on Ashkenazi Jew genealogical projects are included (see Methods for details), the Q3 frequencies in Europe become almost as high as in West Asia (Additional file 1: Figure S1).

David's grandfather, Nathan Abrahm Goldfus, was from Telsiai, Lithuania.  Lithuanian Jews are mostly of :Recent genetic studies, based on Y chromosome polymorphic markers, showed that Ashkenazi Jews are more closely related to other Jewish and Middle Eastern groups than to their host populations in Europe. 

However, Ashkenazim have an elevated frequency of R-M17, the dominant Y chromosome haplogroup in Eastern Europeans, suggesting possible gene flow. In the present study of 495 Y chromosomes of Ashkenazim, 57 (11.5%) were found to belong to R-M17

Detailed analyses of haplotype structure, diversity and geographic distribution suggest a founder effect for this haplogroup, introduced at an early stage into the evolving Ashkenazi community in Europe. R-M17 chromosomes in Ashkenazim may represent vestiges of the mysterious Khazars.  Or, this could show it is from old references.  

Ashkenazi Jews, who have resided in various European countries during the Diaspora, traditionally trace their origin to the Jewish people that lived in the Holy Land before the Roman exile. 

However, some studies claimed that a substantial part of Ashkenazim were descendants of Eastern European non-Jews. In particular, according to Middle Age historians, the Khazars from a small kingdom near the Caspian Sea converted en masse to Judaism and therefore might have contributed to the composition of the emerging Ashkenazi community. 

Yet, recent genetic studies, based on Y chromosome polymorphic markers, clearly showed that Ashkenazim are more closely related to other Jewish and Middle Eastern groups than to their host populations in Europe Those findings argue against large-scale male-mediated gene flow into the Ashkenazi community during the Diaspora. 

The male admixture proportion of Europeans in Ashkenazi Jews was estimated to be 0.5% per generation, indicating that Ashkenazim remained, to a large extent, genetically isolated throughout their history.

Familial hypercholesterolemia (FH) is an autosomal dominant disorder, characterized by markedly elevated plasma concentrations of LDL cholesterol, typically above the 95th percentile for age and sex, caused by mutations in the gene encoding for the low-density lipoprotein receptor (LDLR).

Familial hypercholesterolemia (FH) is an autosomal dominant disease caused by mutations in the low-density-lipoprotein (LDL) receptor. Here we characterize an LDL-receptor founder mutation that is associated with a distinct LDL-receptor haplotype and is responsible for FH in 35% of 71 Jewish-Ashkenazi FH families in Israel. Sixty four percent (16/25) of the Ashkenazi patients who carry this mutant allele were of Lithuanian origin. The mutation was not found in 47 non-Ashkenazi FH families. This mutation was prevalent (8/10 FH cases) in the Jewish community in South Africa, which originated mainly from Lithuania. The mutation, a 3-bp in-frame deletion that would result in the elimination of Gly197, has been previously designated FH-Piscataway. PCR amplification of a DNA fragment that includes the mutation in heterozygous individuals results in the formation of a heteroduplex that can be demonstrated by PAGE and used for molecular diagnosis.

People with FH have increased blood levels of low-density lipoprotein (LDL) cholesterol, sometimes called “bad cholesterol.” Having too much LDL cholesterol in your blood increases your risk for developing coronary artery disease or having a heart attack.

Resource:

https://www.academia.edu/32595370/Phylogeography_of_human_Y_chromosome_haplogroup_Q3_L275_from_an_academic_citizen_science_collaboration

https://www.nature.com/articles/5201319   R-M17

https://www.proquest.com/openview/899bd2e89a5da9defde02fb8dc1db5bd/1?pq-origsite=gscholar&cbl=44659

https://pubmed.ncbi.nlm.nih.gov/1867200/

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