The dichotomous size variation of human complement C4 genes is mediated by a novel family of endogenous retroviruses, which also establishes species-specific genomic patterns among Old World primates

1994 ◽  
Vol 40 (6) ◽  
Author(s):  
AndrewW. Dangel ◽  
AnnaR. Mendoza ◽  
C.D. Menachery ◽  
BradleyJ. Baker ◽  
CharlesM. Daniel ◽  
...  
2020 ◽  
Vol 27 (10) ◽  
pp. 967-977 ◽  
Author(s):  
Akihiko Sakashita ◽  
So Maezawa ◽  
Kazuki Takahashi ◽  
Kris G. Alavattam ◽  
Masashi Yukawa ◽  
...  

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Aaron B. Bogutz ◽  
Julie Brind’Amour ◽  
Hisato Kobayashi ◽  
Kristoffer N. Jensen ◽  
Kazuhiko Nakabayashi ◽  
...  

AbstractImprinted genes are expressed from a single parental allele, with the other allele often silenced by DNA methylation (DNAme) established in the germline. While species-specific imprinted orthologues have been documented, the molecular mechanisms underlying the evolutionary switch from biallelic to imprinted expression are unknown. During mouse oogenesis, gametic differentially methylated regions (gDMRs) acquire DNAme in a transcription-guided manner. Here we show that oocyte transcription initiating in lineage-specific endogenous retroviruses (ERVs) is likely responsible for DNAme establishment at 4/6 mouse-specific and 17/110 human-specific imprinted gDMRs. The latter are divided into Catarrhini- or Hominoidea-specific gDMRs embedded within transcripts initiating in ERVs specific to these primate lineages. Strikingly, imprinting of the maternally methylated genes Impact and Slc38a4 was lost in the offspring of female mice harboring deletions of the relevant murine-specific ERVs upstream of these genes. Our work reveals an evolutionary mechanism whereby maternally silenced genes arise from biallelically expressed progenitors.


1985 ◽  
Vol 5 (10-11) ◽  
pp. 913-921 ◽  
Author(s):  
S. K. Alex Law ◽  
Jean Gagnon

C-terminal CNBr peptides of the three polypeptide chains of C4 were obtained and sequenced. These results supplement previously obtained data, notably the protein sequence derived from cDNA sequencing of pro-C4 (Belt KT, Carroll MC & Porter RR (1984) Cell36, 907–914) and the N-terminal sequences of the three polypeptides (Gigli I, von Zabern I & Porter RR (1977) Biochem. J.165, 439–446), to define the complete primary structure of the plasma form of C4. The β (656 residues), α (748 residues), and γ (291 residues) chains are found in positions 1–656, 661–1408, and 1435–1725 in the pro-C4 molecule.


2005 ◽  
Vol 79 (18) ◽  
pp. 12035-12044 ◽  
Author(s):  
Stephen D. Barr ◽  
Jeremy Leipzig ◽  
Paul Shinn ◽  
Joe R. Ecker ◽  
Frederic D. Bushman

ABSTRACT We have analyzed the placement of sites of integration of avian sarcoma-leukosis virus (ASLV) and human immunodeficiency virus (HIV) DNA in the draft chicken genome sequence, with the goals of assessing species-specific effects on integration and allowing comparison to the distribution of chicken endogenous retroviruses (ERVs). We infected chicken embryo fibroblasts (CEF) with ASLV or HIV and sequenced 863 junctions between host and viral DNA. The relationship with cellular gene activity was analyzed by transcriptional profiling of uninfected or ASLV-infected CEF cells. ASLV weakly favored integration in active transcription units (TUs), and HIV strongly favored active TUs, trends seen previously for integration in human cells. The ERVs, in contrast, accumulated mostly outside TUs, including ERVs related to ASLV. The minority of ERVs present within TUs were mainly in the antisense orientation; consequently, the viral splicing and polyadenylation signals would not disrupt cellular mRNA synthesis. In contrast, de novo ASLV integration sites within TUs showed no orientation bias. Comparing the distribution of de novo ASLV integration sites to ERVs indicated that purifying selection against gene disruption, and not initial integration targeting, probably determined the ERV distribution. Further analysis indicated that ERVs in humans, mice, and rats showed similar distributions, suggesting purifying selection dictated their distributions as well.


2001 ◽  
Vol 18 (3) ◽  
pp. 130-134 ◽  
Author(s):  
Peter M. Schneider ◽  
Konstanze Witzel-Schlömp ◽  
Constanze Steinhauer ◽  
Beate Stradmann-Bellinghausen ◽  
Christian Rittner

2013 ◽  
Vol 288 (22) ◽  
pp. 15821-15829 ◽  
Author(s):  
Andrew J. Perry ◽  
Lakshmi C. Wijeyewickrema ◽  
Pascal G. Wilmann ◽  
Menachem J. Gunzburg ◽  
Laura D'Andrea ◽  
...  

2013 ◽  
Vol 45 (3) ◽  
pp. 325-329 ◽  
Author(s):  
Edward B Chuong ◽  
M A Karim Rumi ◽  
Michael J Soares ◽  
Julie C Baker

1992 ◽  
Vol 175 (2) ◽  
pp. 537-543 ◽  
Author(s):  
O Finco ◽  
S Li ◽  
M Cuccia ◽  
F S Rosen ◽  
M C Carroll

An animal model has been used to address the question of the biological importance of the known structural difference between the two isotypes of human C4, i.e., C4A and C4B. Guinea pigs deficient in C4 were reconstituted transiently with either human C4A or C4B protein and immunized with the bacteriophage phi X174. Results from this study showed that C4A-reconstituted animals made a secondary response, i.e., switch from IgM to IgG; whereas the C4B-reconstituted animals did not.


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