ALBERT

Description: Throughout evolution primate genomes have been modified by waves of retrotransposon insertions. For each wave, the host eventually finds a way to repress retrotransposon transcription and prevent further insertions. In mouse embryonic stem cells, transcriptional silencing of retrotransposons requires KAP1 (also known as TRIM28) and its repressive complex, which can be recruited to target sites by KRAB zinc-finger (KZNF) proteins such as murine-specific ZFP809 which binds to integrated murine leukaemia virus DNA elements and recruits KAP1 to repress them. KZNF genes are one of the fastest growing gene families in primates and this expansion is hypothesized to enable primates to respond to newly emerged retrotransposons. However, the identity of KZNF genes battling retrotransposons currently active in the human genome, such as SINE-VNTR-Alu (SVA) and long interspersed nuclear element 1 (L1), is unknown. Here we show that two primate-specific KZNF genes rapidly evolved to repress these two distinct retrotransposon families shortly after they began to spread in our ancestral genome. ZNF91 underwent a series of structural changes 8-12 million years ago that enabled it to repress SVA elements. ZNF93 evolved earlier to repress the primate L1 lineage until approximately 12.5 million years ago when the L1PA3-subfamily of retrotransposons escaped ZNF93's restriction through the removal of the ZNF93-binding site. Our data support a model where KZNF gene expansion limits the activity of newly emerged retrotransposon classes, and this is followed by mutations in these retrotransposons to evade repression, a cycle of events that could explain the rapid expansion of lineage-specific KZNF genes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4268317/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4268317/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jacobs, Frank M J -- Greenberg, David -- Nguyen, Ngan -- Haeussler, Maximilian -- Ewing, Adam D -- Katzman, Sol -- Paten, Benedict -- Salama, Sofie R -- Haussler, David -- U24 CA143858/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Dec 11;516(7530):242-5. doi: 10.1038/nature13760. Epub 2014 Sep 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Center for Biomolecular Science and Engineering, University of California Santa Cruz, Santa Cruz, California 95064, USA [2] [3] Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam 1098 XH, The Netherlands (F.M.J.J.); Gladstone Institute of Virology and Immunology, San Francisco, California 94158, USA (D.G.); Mater Research Institute, University of Queensland, Queensland 4101, Australia (A.D.E.). ; 1] Center for Biomolecular Science and Engineering, University of California Santa Cruz, Santa Cruz, California 95064, USA [2] Molecular, Cell and Developmental Biology, University of California Santa Cruz, Santa Cruz, California 95064, USA [3] [4] Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam 1098 XH, The Netherlands (F.M.J.J.); Gladstone Institute of Virology and Immunology, San Francisco, California 94158, USA (D.G.); Mater Research Institute, University of Queensland, Queensland 4101, Australia (A.D.E.). ; 1] Center for Biomolecular Science and Engineering, University of California Santa Cruz, Santa Cruz, California 95064, USA [2] Biomolecular Engineering, University of California Santa Cruz, Santa Cruz, California 95064, USA. ; Center for Biomolecular Science and Engineering, University of California Santa Cruz, Santa Cruz, California 95064, USA. ; 1] Center for Biomolecular Science and Engineering, University of California Santa Cruz, Santa Cruz, California 95064, USA [2] Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam 1098 XH, The Netherlands (F.M.J.J.); Gladstone Institute of Virology and Immunology, San Francisco, California 94158, USA (D.G.); Mater Research Institute, University of Queensland, Queensland 4101, Australia (A.D.E.). ; 1] Center for Biomolecular Science and Engineering, University of California Santa Cruz, Santa Cruz, California 95064, USA [2] Howard Hughes Medical Institute, University of California Santa Cruz, Santa Cruz, California 95064, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25274305" target="_blank"〉PubMed〈/a〉

Description: Ultraconserved elements in the human genome are defined as stretches of at least 200 base pairs of DNA that match identically with corresponding regions in the mouse and rat genomes. Most ultraconserved elements are noncoding and have been evolutionarily conserved since mammal and bird ancestors diverged over 300 million years ago. The reason for this extreme conservation remains a mystery. It has been speculated that they are mutational cold spots or regions where every site is under weak but still detectable negative selection. However, analysis of the derived allele frequency spectrum shows that these regions are in fact under negative selection that is much stronger than that in protein coding genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Katzman, Sol -- Kern, Andrew D -- Bejerano, Gill -- Fewell, Ginger -- Fulton, Lucinda -- Wilson, Richard K -- Salama, Sofie R -- Haussler, David -- New York, N.Y. -- Science. 2007 Aug 17;317(5840):915.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomolecular Engineering, University of California, Santa Cruz, CA 95064, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17702936" target="_blank"〉PubMed〈/a〉

Description: The transfer of the human gene for hypoxanthine phosphoribosyltransferase (HPRT) into human bone marrow cells was accomplished by use of a retroviral vector. The cells were infected in vitro with a replication-incompetent murine retroviral vector that carried and expressed a mutant HPRT complementary DNA. The infected cells were superinfected with a helper virus and maintained in long-term culture. The production of progeny HPRT virus by the bone marrow cells was demonstrated with a colony formation assay on cultured HPRT-deficient, ouabain-resistant murine fibroblasts. Hematopoietic progenitor cells able to form colonies of granulocytes or macrophages (or both) in semisolid medium in the presence of colony stimulating factor were present in the nonadherent cell population. Colony forming units cloned in agar and subsequently cultured in liquid medium produced progeny HPRT virus, indicating infection of this class of hematopoietic progenitor cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gruber, H E -- Finley, K D -- Hershberg, R M -- Katzman, S S -- Laikind, P K -- Seegmiller, J E -- Friedmann, T -- Yee, J K -- Jolly, D J -- AM 13622/AM/NIADDK NIH HHS/ -- GM 28223/GM/NIGMS NIH HHS/ -- HD20034/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Nov 29;230(4729):1057-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3864246" target="_blank"〉PubMed〈/a〉

Description: Generation of distinct cortical projection neuron subtypes during development relies in part on repression of alternative neuron identities. It was reported that the special AT-rich sequence-binding protein 2 (Satb2) is required for proper development of callosal neuron identity and represses expression of genes that are essential for subcerebral axon development....