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Frank M J Jacobs - One of the best experts on this subject based on the ideXlab platform.
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an evolutionary arms race between krab zinc finger genes znf91 93 and sva l1 Retrotransposons
Nature, 2014Co-Authors: Frank M J Jacobs, David Greenberg, Ngan Nguyen, Maximilian Haeussler, Adam D Ewing, Sol Katzman, Benedict PatenAbstract: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 ∼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.
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an evolutionary arms race between krab zinc finger genes znf91 93 and sva l1 Retrotransposons
Nature, 2014Co-Authors: Frank M J Jacobs, David Greenberg, Ngan Nguyen, Maximilian Haeussler, Adam D Ewing, Sol Katzman, Benedict PatenAbstract:The authors show that two primate-specific genes encoding KRAB domain containing zinc finger proteins, ZNF91 and ZNF93, have evolved during the last 25 million years to repress retrotransposon families that emerged during this time period; according to the new data KZNF gene expansion limits the activity of newly emerged Retrotransposons, which subsequently mutate to evade repression. Primate genomes have endured waves of retrotransposon insertions despite the host's attempts to prevent them and to block their transcription. KRAB domain containing zinc-finger proteins (KZNFs) plays a role in this transcriptional silencing in mouse embryonic stem cells. KZNFs are one of the fastest growing gene families in primates; this expansion has been hypothesized to enable primates to respond to newly emerged transposable elements. Here the authors provide evidence in support of this theory. They show that two primate-specific KZNF genes, ZNF91 and ZNF93, have evolved during the past 25 million years to repress distinct retrotransposon families that emerged during this time period. According to the new data, KZNF gene expansion limits the activity of newly emerged Retrotransposons, which subsequently mutate to evade repression. Throughout evolution primate genomes have been modified by waves of retrotransposon insertions1,2,3. 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 them4,5. 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 Retrotransposons6,7. However, the identity of KZNF genes battling Retrotransposons currently active in the human genome, such as SINE-VNTR-Alu (SVA)8 and long interspersed nuclear element 1 (L1)9, 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 ∼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.
Alan H Schulman - One of the best experts on this subject based on the ideXlab platform.
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The Tvv1 retrotransposon family is conserved between plant genomes separated by over 100 million years
TAG Theoretical and Applied Genetics, 2014Co-Authors: Cedric Moisy, Jan P. Buchmann, Ruslan Kalendar, Alan H Schulman, Frédérique PelsyAbstract:Abstract Key message Combining several different approaches, we have examined the structure, variability, and distribution of Tvv1 Retrotransposons. Tvv1 is an unusual example of a low-copy retrotransposon metapopulation dispersed unevenly among very distant species and is promising for the development of molecular markers. Retrotransposons are ubiquitous throughout the genomes of the vascular plants, but individual retrotransposon families tend to be confined to the level of plant genus or at most family. This restricts the general applicability of a family as molecular markers. Here, we characterize a new plant retrotransposon named Tvv1_Sdem, a member of the Copia superfamily of LTR Retrotransposons, from the genome of the wild potato Solanum demissum. Comparative analyses based on structure and sequence showed a high level of similarity of Tvv1_Sdem with Tvv1-VB, a retrotransposon previously described in the grapevine genome Vitis vinifera. Extending the analysis to other species by in silico and in vitro approaches revealed the presence of Tvv1 family members in potato, tomato, and poplar genomes, and led to the identification of full-length copies of Tvv1 in these species. We were also able to identify polymorphism in UTL sequences between Tvv1_Sdem copies from wild and cultivated potatoes that are useful as molecular markers. Combining different approaches, our results suggest that the Tvv1 family of Retrotransposons has a monophyletic origin and has been maintained in both the rosids and the asterids, the major clades of dicotyledonous plants, since their divergence about 100 MYA. To our knowledge, Tvv1 represents an unusual plant retrotransposon metapopulation comprising highly similar members disjointedly dispersed among very distant species. The twin features of Tvv1 presence in evolutionarily distant genomes and the diversity of its UTL region in each species make it useful as a source of robust molecular markers for diversity studies and breeding.
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Retrotransposon replication in plants
Current Opinion in Virology, 2013Co-Authors: Alan H SchulmanAbstract:Retrotransposons comprise the bulk of large plant genomes, replicating via an RNA intermediate whereby the original, integrated element remains in place. Of the two main orders, the LTR Retrotransposons considerably outnumber the LINEs. LINEs integrate into target sites simultaneously with the RNA transcript being copied into cDNA by target-primed reverse transcription. LTR retrotransposon replication is basically equivalent to the intracellular phase of retroviral life cycles. The envelope gene giving extracellular mobility to retroviruses is in fact widespread in plants and their Retrotransposons. Evolutionary analyses of the Retrotransposons and retroviruses suggest that both form an ancient monophyletic group. The particular adaptations of LTR Retrotransposons to plant life cycles enabling their success remain to be clarified.
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Hitching a Ride: Nonautonomous Retrotransposons and Parasitism as a Lifestyle
Plant Transposable Elements, 2012Co-Authors: Alan H SchulmanAbstract:Large genomes in plants are composed primarily of long terminal repeat (LTR) Retrotransposons, which replicate and propagate by a “copy-and-paste” mechanism dependent on enzymes encoded by the Retrotransposons themselves. The enzymes direct a life cycle involving transcription, translation, packaging, reverse transcription, and integration. Loss of any coding capacity will render a retrotransposon incapable of completing its life cycle autonomously. Nevertheless, Retrotransposons lacking complete open reading frames for one or more of their proteins are abundant in the genome. These nonautonomous Retrotransposons can, however, be complemented in trans by proteins expressed by another retrotransposon, restoring mobility. It is sufficient for a nonautonomous LTR retrotransposon to retain the signals needed for recognition by the transcription machinery and the proteins of autonomous elements. The degree to which nonautonomous Retrotransposons interfere with the propagation of autonomous elements has major evolutionary consequences for the genome, affecting the relative rate of gain versus loss of Retrotransposons and thereby genome size.
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analysis of plant diversity with retrotransposon based molecular markers
Heredity, 2011Co-Authors: Ruslan Kalendar, Andrew J. Flavell, T H N Ellis, Tatjana Sjakste, Cedric Moisy, Alan H SchulmanAbstract:Retrotransposons are both major generators of genetic diversity and tools for detecting the genomic changes associated with their activity because they create large and stable insertions in the genome. After the demonstration that Retrotransposons are ubiquitous, active and abundant in plant genomes, various marker systems were developed to exploit polymorphisms in retrotransposon insertion patterns. These have found applications ranging from the mapping of genes responsible for particular traits and the management of backcrossing programs to analysis of population structure and diversity of wild species. This review provides an insight into the spectrum of retrotransposon-based marker systems developed for plant species and evaluates the contributions of retrotransposon markers to the analysis of population diversity in plants.
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iPBS: a universal method for DNA fingerprinting and retrotransposon isolation
Theoretical and Applied Genetics, 2010Co-Authors: Ruslan Kalendar, Kristiina Antonius, Petr Smýkal, Alan H SchulmanAbstract:Molecular markers are essential in plant and animal breeding and biodiversity applications, in human forensics, and for map-based cloning of genes. The long terminal repeat (LTR) Retrotransposons are well suited as molecular markers. As dispersed and ubiquitous transposable elements, their “copy and paste” life cycle of replicative transposition leads to new genome insertions without excision of the original element. Both the overall structure of Retrotransposons and the domains responsible for the various phases of their replication are highly conserved in all eukaryotes. Nevertheless, up to a year has been required to develop a retrotransposon marker system in a new species, involving cloning and sequencing steps as well as the development of custom primers. Here, we describe a novel PCR-based method useful both as a marker system in its own right and for the rapid isolation of retrotransposon termini and full-length elements, making it ideal for “orphan crops” and other species with underdeveloped marker systems. The method, iPBS amplification, is based on the virtually universal presence of a tRNA complement as a reverse transcriptase primer binding site (PBS) in LTR Retrotransposons. The method differs from earlier retrotransposon isolation methods because it is applicable not only to endogenous retroviruses and retroviruses, but also to both Gypsy and Copia LTR Retrotransposons, as well as to non-autonomous LARD and TRIM elements, throughout the plant kingdom and to animals. Furthermore, the inter-PBS amplification technique as such has proved to be a powerful DNA fingerprinting technology without the need for prior sequence knowledge.
Benedict Paten - One of the best experts on this subject based on the ideXlab platform.
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an evolutionary arms race between krab zinc finger genes znf91 93 and sva l1 Retrotransposons
Nature, 2014Co-Authors: Frank M J Jacobs, David Greenberg, Ngan Nguyen, Maximilian Haeussler, Adam D Ewing, Sol Katzman, Benedict PatenAbstract: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 ∼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.
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an evolutionary arms race between krab zinc finger genes znf91 93 and sva l1 Retrotransposons
Nature, 2014Co-Authors: Frank M J Jacobs, David Greenberg, Ngan Nguyen, Maximilian Haeussler, Adam D Ewing, Sol Katzman, Benedict PatenAbstract:The authors show that two primate-specific genes encoding KRAB domain containing zinc finger proteins, ZNF91 and ZNF93, have evolved during the last 25 million years to repress retrotransposon families that emerged during this time period; according to the new data KZNF gene expansion limits the activity of newly emerged Retrotransposons, which subsequently mutate to evade repression. Primate genomes have endured waves of retrotransposon insertions despite the host's attempts to prevent them and to block their transcription. KRAB domain containing zinc-finger proteins (KZNFs) plays a role in this transcriptional silencing in mouse embryonic stem cells. KZNFs are one of the fastest growing gene families in primates; this expansion has been hypothesized to enable primates to respond to newly emerged transposable elements. Here the authors provide evidence in support of this theory. They show that two primate-specific KZNF genes, ZNF91 and ZNF93, have evolved during the past 25 million years to repress distinct retrotransposon families that emerged during this time period. According to the new data, KZNF gene expansion limits the activity of newly emerged Retrotransposons, which subsequently mutate to evade repression. Throughout evolution primate genomes have been modified by waves of retrotransposon insertions1,2,3. 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 them4,5. 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 Retrotransposons6,7. However, the identity of KZNF genes battling Retrotransposons currently active in the human genome, such as SINE-VNTR-Alu (SVA)8 and long interspersed nuclear element 1 (L1)9, 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 ∼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.
David Greenberg - One of the best experts on this subject based on the ideXlab platform.
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an evolutionary arms race between krab zinc finger genes znf91 93 and sva l1 Retrotransposons
Nature, 2014Co-Authors: Frank M J Jacobs, David Greenberg, Ngan Nguyen, Maximilian Haeussler, Adam D Ewing, Sol Katzman, Benedict PatenAbstract: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 ∼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.
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an evolutionary arms race between krab zinc finger genes znf91 93 and sva l1 Retrotransposons
Nature, 2014Co-Authors: Frank M J Jacobs, David Greenberg, Ngan Nguyen, Maximilian Haeussler, Adam D Ewing, Sol Katzman, Benedict PatenAbstract:The authors show that two primate-specific genes encoding KRAB domain containing zinc finger proteins, ZNF91 and ZNF93, have evolved during the last 25 million years to repress retrotransposon families that emerged during this time period; according to the new data KZNF gene expansion limits the activity of newly emerged Retrotransposons, which subsequently mutate to evade repression. Primate genomes have endured waves of retrotransposon insertions despite the host's attempts to prevent them and to block their transcription. KRAB domain containing zinc-finger proteins (KZNFs) plays a role in this transcriptional silencing in mouse embryonic stem cells. KZNFs are one of the fastest growing gene families in primates; this expansion has been hypothesized to enable primates to respond to newly emerged transposable elements. Here the authors provide evidence in support of this theory. They show that two primate-specific KZNF genes, ZNF91 and ZNF93, have evolved during the past 25 million years to repress distinct retrotransposon families that emerged during this time period. According to the new data, KZNF gene expansion limits the activity of newly emerged Retrotransposons, which subsequently mutate to evade repression. Throughout evolution primate genomes have been modified by waves of retrotransposon insertions1,2,3. 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 them4,5. 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 Retrotransposons6,7. However, the identity of KZNF genes battling Retrotransposons currently active in the human genome, such as SINE-VNTR-Alu (SVA)8 and long interspersed nuclear element 1 (L1)9, 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 ∼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.
Adam D Ewing - One of the best experts on this subject based on the ideXlab platform.
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an evolutionary arms race between krab zinc finger genes znf91 93 and sva l1 Retrotransposons
Nature, 2014Co-Authors: Frank M J Jacobs, David Greenberg, Ngan Nguyen, Maximilian Haeussler, Adam D Ewing, Sol Katzman, Benedict PatenAbstract: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 ∼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.
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an evolutionary arms race between krab zinc finger genes znf91 93 and sva l1 Retrotransposons
Nature, 2014Co-Authors: Frank M J Jacobs, David Greenberg, Ngan Nguyen, Maximilian Haeussler, Adam D Ewing, Sol Katzman, Benedict PatenAbstract:The authors show that two primate-specific genes encoding KRAB domain containing zinc finger proteins, ZNF91 and ZNF93, have evolved during the last 25 million years to repress retrotransposon families that emerged during this time period; according to the new data KZNF gene expansion limits the activity of newly emerged Retrotransposons, which subsequently mutate to evade repression. Primate genomes have endured waves of retrotransposon insertions despite the host's attempts to prevent them and to block their transcription. KRAB domain containing zinc-finger proteins (KZNFs) plays a role in this transcriptional silencing in mouse embryonic stem cells. KZNFs are one of the fastest growing gene families in primates; this expansion has been hypothesized to enable primates to respond to newly emerged transposable elements. Here the authors provide evidence in support of this theory. They show that two primate-specific KZNF genes, ZNF91 and ZNF93, have evolved during the past 25 million years to repress distinct retrotransposon families that emerged during this time period. According to the new data, KZNF gene expansion limits the activity of newly emerged Retrotransposons, which subsequently mutate to evade repression. Throughout evolution primate genomes have been modified by waves of retrotransposon insertions1,2,3. 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 them4,5. 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 Retrotransposons6,7. However, the identity of KZNF genes battling Retrotransposons currently active in the human genome, such as SINE-VNTR-Alu (SVA)8 and long interspersed nuclear element 1 (L1)9, 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 ∼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.
