Skip to main content

Thank you for visiting You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Letter
  • Published:

An evolutionary arms race between KRAB zinc-finger genes ZNF91/93 and SVA/L1 retrotransposons


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.

This is a preview of subscription content, access via your institution

Access options

Buy this article

Prices may be subject to local taxes which are calculated during checkout

Figure 1: SVAs and L1PAs are derepressed in a non-primate cellular environment.
Figure 2: SVA elements are repressed by primate-specific ZNF91.
Figure 3: L1PA elements are repressed by primate-specific ZNF93.
Figure 4: Dynamic patterns of co-evolution between ZNFs and target retrotransposons.

Similar content being viewed by others

Accession codes

Primary accessions

Gene Expression Omnibus

Data deposits

The data discussed in this publication have been deposited in the NCBI Gene Expression Omnibus and are accessible through GEO Series accession number GSE60211.


  1. Kazazian, H. H. Mobile elements: drivers of genome evolution. Science 303, 1626–1632 (2004)

    ADS  CAS  PubMed  Google Scholar 

  2. Cordaux, R. & Batzer, M. A. The impact of retrotransposons on human genome evolution. Nature Rev. Genet. 10, 691–703 (2009)

    CAS  PubMed  Google Scholar 

  3. Lander, E. S. et al. Initial sequencing and analysis of the human genome. Nature 409, 860–921 (2001)

    ADS  CAS  PubMed  Google Scholar 

  4. Wolf, D. & Goff, S. P. TRIM28 mediates primer binding site-targeted silencing of murine leukemia virus in embryonic cells. Cell 131, 46–57 (2007)

    CAS  PubMed  Google Scholar 

  5. Wolf, D. & Goff, S. P. Embryonic stem cells use ZFP809 to silence retroviral DNAs. Nature 458, 1201–1204 (2009)

    ADS  CAS  PubMed  PubMed Central  Google Scholar 

  6. Birtle, Z. & Ponting, C. P. Meisetz and the birth of the KRAB motif. Bioinformatics 22, 2841–2845 (2006)

    CAS  PubMed  Google Scholar 

  7. Thomas, J. H. & Schneider, S. Coevolution of retroelements and tandem zinc finger genes. Genome Res. 21, 1800–1812 (2011)

    CAS  PubMed  PubMed Central  Google Scholar 

  8. Wang, H. et al. SVA elements: a hominid-specific retroposon family. J. Mol. Biol. 354, 994–1007 (2005)

    CAS  PubMed  Google Scholar 

  9. Khan, H., Smit, A. & Boissinot, S. Molecular evolution and tempo of amplification of human LINE-1 retrotransposons since the origin of primates. Genome Res. 16, 78–87 (2006)

    CAS  PubMed  PubMed Central  Google Scholar 

  10. Rowe, H. M. et al. KAP1 controls endogenous retroviruses in embryonic stem cells. Nature 463, 237–240 (2010)

    ADS  CAS  PubMed  Google Scholar 

  11. Turelli, P. et al. Interplay of TRIM28 and DNA methylation in controlling human endogenous retroelements. Genome Res. 24, 1260–1270 (2014)

    CAS  PubMed  PubMed Central  Google Scholar 

  12. Castro-Diaz, N. et al. Evolutionally dynamic L1 regulation in embryonic stem cells. Genes Dev. 28, 1397–1409 (2014)

    CAS  PubMed  PubMed Central  Google Scholar 

  13. Huntley, S. et al. A comprehensive catalog of human KRAB-associated zinc finger genes: insights into the evolutionary history of a large family of transcriptional repressors. Genome Res. 16, 669–677 (2006)

    CAS  PubMed  PubMed Central  Google Scholar 

  14. Kai, Y. et al. Enhanced apoptosis during early neuronal differentiation in mouse ES cells with autosomal imbalance. Cell Res. 19, 247–258 (2009)

    CAS  PubMed  Google Scholar 

  15. Gifford, W. D., Pfaff, S. L. & Macfarlan, T. S. Transposable elements as genetic regulatory substrates in early development. Trends Cell Biol. 23, 218–226 (2013)

    CAS  PubMed  PubMed Central  Google Scholar 

  16. Ward, M. C. et al. Latent regulatory potential of human-specific repetitive elements. Mol. Cell 49, 262–272 (2013)

    CAS  PubMed  PubMed Central  Google Scholar 

  17. Hancks, D. C. & Kazazian, H. H. Active human retrotransposons: variation and disease. Curr. Opin. Genet. Dev. 22, 191–203 (2012)

    CAS  PubMed  PubMed Central  Google Scholar 

  18. Bellefroid, E. J. et al. Emergence of the ZNF91 Krüppel-associated box-containing zinc finger gene family in the last common ancestor of anthropoidea. Proc. Natl Acad. Sci. USA 92, 10757–10761 (1995)

    ADS  CAS  PubMed  PubMed Central  Google Scholar 

  19. Levin, H. L. & Moran, J. V. Dynamic interactions between transposable elements and their hosts. Nature Rev. Genet. 12, 615–627 (2011)

    CAS  PubMed  Google Scholar 

  20. Persikov, A. V., Osada, R. & Singh, M. Predicting DNA recognition by Cys2His2 zinc finger proteins. Bioinformatics 25, 22–29 (2009)

    CAS  PubMed  Google Scholar 

  21. Moore, M., Choo, Y. & Klug, A. Design of polyzinc finger peptides with structured linkers. Proc. Natl Acad. Sci. USA 98, 1432–1436 (2001)

    ADS  CAS  PubMed  PubMed Central  Google Scholar 

  22. Ostertag, E. M., Prak, E. T., DeBerardinis, R. J., Moran, J. V. & Kazazian, H. H. Determination of L1 retrotransposition kinetics in cultured cells. Nucleic Acids Res. 28, 1418–1423 (2000)

    CAS  PubMed  PubMed Central  Google Scholar 

  23. Kimberland, M. L. et al. Full-length human L1 insertions retain the capacity for high frequency retrotransposition in cultured cells. Hum. Mol. Genet. 8, 1557–1560 (1999)

    CAS  PubMed  Google Scholar 

  24. Swergold, G. D. Identification, characterization, and cell specificity of a human LINE-1 promoter. Mol. Cell. Biol. 10, 6718–6729 (1990)

    CAS  PubMed  PubMed Central  Google Scholar 

  25. Lowe, C. B., Bejerano, G. & Haussler, D. Thousands of human mobile element fragments undergo strong purifying selection near developmental genes. Proc. Natl Acad. Sci. USA 104, 8005–8010 (2007)

    ADS  CAS  PubMed  PubMed Central  Google Scholar 

  26. Parkhomchuk, D. et al. Transcriptome analysis by strand-specific sequencing of complementary DNA. Nucleic Acids Res. 37, e123 (2009)

    PubMed  PubMed Central  Google Scholar 

  27. Kim, D. et al. TopHat2: accurate alignment of transcriptomes in the presence of insertions, deletions and gene fusions. Genome Biol. 14, R36 (2013)

    PubMed  PubMed Central  Google Scholar 

  28. Langmead, B. & Salzberg, S. L. Fast gapped-read alignment with Bowtie 2. Nature Methods 9, 357–359 (2012)

    CAS  PubMed  PubMed Central  Google Scholar 

  29. Hsu, F. et al. The UCSC known genes. Bioinformatics 22, 1036–1046 (2006)

    CAS  PubMed  Google Scholar 

  30. Li, H. et al. The sequence alignment/map format and SAMtools. Bioinformatics 25, 2078–2079 (2009)

    Article  PubMed  PubMed Central  Google Scholar 

  31. Quinlan, A. R. & Hall, I. M. BEDTools: a flexible suite of utilities for comparing genomic features. Bioinformatics 26, 841–842 (2010)

    CAS  PubMed  PubMed Central  Google Scholar 

  32. Anders, S. & Huber, W. Differential expression analysis for sequence count data. Genome Biol. 11, R106 (2010)

    CAS  PubMed  PubMed Central  Google Scholar 

  33. Zhang, Y. et al. Model-based analysis of ChIP-Seq (MACS). Genome Biol. 9, R137 (2008)

    PubMed  PubMed Central  Google Scholar 

  34. Onodera, C. S. et al. Gene isoform specificity through enhancer-associated antisense transcription. PLoS ONE 7, e43511 (2012)

    ADS  CAS  PubMed  PubMed Central  Google Scholar 

  35. Ying, Q.-L., Stavridis, M., Griffiths, D., Li, M. & Smith, A. Conversion of embryonic stem cells into neuroectodermal precursors in adherent monoculture. Nature Biotechnol. 21, 183–186 (2003)

    CAS  Google Scholar 

  36. Hancks, D. C., Mandal, P. K., Cheung, L. E. & Kazazian, H. H. The minimal active human SVA retrotransposon requires only the 5′-hexamer and Alu-like domains. Mol. Cell. Biol. 32, 4718–4726 (2012)

    CAS  PubMed  PubMed Central  Google Scholar 

  37. Kent, W. J. et al. The human genome browser at UCSC. Genome Res. 12, 996–1006 (2002)

    CAS  PubMed  PubMed Central  Google Scholar 

  38. Löytynoja, A. & Goldman, N. Phylogeny-aware gap placement prevents errors in sequence alignment and evolutionary analysis. Science 320, 1632–1635 (2008)

    ADS  PubMed  Google Scholar 

  39. Edgar, R. C. MUSCLE: multiple sequence alignment with high accuracy and high throughput. Nucleic Acids Res. 32, 1792–1797 (2004)

    CAS  PubMed  PubMed Central  Google Scholar 

  40. Katoh, K. & Standley, D. M. MAFFT multiple sequence alignment software version 7: improvements in performance and usability. Mol. Biol. Evol. 30, 772–780 (2013)

    CAS  PubMed  PubMed Central  Google Scholar 

  41. Tamura, K., Stecher, G., Peterson, D., Filipski, A. & Kumar, S. MEGA6: molecular evolutionary genetics analysis version 6.0. Mol. Biol. Evol. 30, 2725–2729 (2013)

    CAS  PubMed  PubMed Central  Google Scholar 

  42. Rzhetsky, A. & Nei, M. A simple method for estimating and testing minimum-evolution trees. Mol. Biol. Evol. 9, 945–967 (1992)

    CAS  Google Scholar 

  43. Tamura, K. et al. Estimating divergence times in large molecular phylogenies. Proc. Natl Acad. Sci. USA 109, 19333–19338 (2012)

    ADS  CAS  PubMed  PubMed Central  Google Scholar 

  44. Benson, G. Tandem repeats finder: a program to analyze DNA sequences. Nucleic Acids Res. 27, 573–580 (1999)

    CAS  PubMed  PubMed Central  Google Scholar 

  45. Naas, T. P. et al. An actively retrotransposing, novel subfamily of mouse L1 elements. EMBO J. 17, 590–597 (1998)

    CAS  PubMed  PubMed Central  Google Scholar 

Download references


This work was supported by California Institute of Regenerative Medicine (CIRM) facility awards (FA1-00617, CL1-00506-1.2) and scholar awards (TG2-01157) to F.M.J.J. and D.G. and F.M.J.J. also received a Human Frontier Science Program Postdoctoral fellowship (LT000689). D.H. is an Investigator of the Howard Hughes Medical Institute. S.K. is supported by the California Institute for Quantitative Biosciences, A.D.E. was supported by TCGA U24 24010-443720, M.H. by EMBO ALTF 292-2011, and B.P. and N.N. by ENCODE U41HG004568. We thank F. Wianny and C. Dehay (Lyon University) for the LYON-ES1 macaque embryonic stem cells; M. Oshimura and T. Inoue (Tottori University) for the E14(hChr11) trans-chromosomic embryonic stem cells, N. Pourmand and the UCSC genome sequencing center; B. Nazario (UCSC Institute for the Biology of Stem Cells) for flow cytometry assistance; M. Batzer (LSU) and K. Han (Dankook University) for L1CER sequences; L. Carbone (OHSU) for gibbon genomic DNA; A. Smit (ISB, Seattle) for discussions on L1PA evolution; D. Segal (UC Davis) for advice on ZNF mutations; H. Kazazian, D. Hancks and J. Goodier (JHMI) for retrotransposition plasmids and advice; K. Tygi, C. Vizenor, J. Rosenkrantz, W. Novey, S. Kyane and B. Mylenek for technical assistance and the entire Haussler laboratory for discussions and support.

Author information

Authors and Affiliations



F.M.J.J., D.G., D.H. and S.R.S. designed and analysed the experiments. F.M.J.J. performed RNA-seq, ChIP-seq and reintroduction of primate ZNFs in trans-chromosomic mESCs; D.G. performed ZNF cloning, luciferase reporter and retrotransposition assays; N.N., D.G., A.D.E. and B.P. performed resequencing and analysis to complete the ZNF91 and ZNF93 loci in various primates; N.N. and B.P. reconstructed the evolutionary history of ZNF91 and ZNF93 ZNF domains; M.H. generated a Repeatmasker UCSC-Browser and hub, ZNF-binding site predictions and VNTR length analysis; S.K. processed and analysed RNA-seq and ChIP-seq data; A.D.E. analysed SVA numbers in great apes and SVA–gene-expression correlations. F.M.J.J., D.G., S.R.S. and D.H. wrote the manuscript.

Corresponding author

Correspondence to David Haussler.

Ethics declarations

Competing interests

The authors declare no competing financial interests.

Extended data figures and tables

Extended Data Figure 1 KAP1 associates with recently emerged transposable elements.

a, Immunoblot incubated with anti-KAP1 antibody loaded with 1% input and eluates of KAP1-ChIP or IgG-ChIP derived from hESC lysates. b, Diagram showing numbers of KAP1 peaks identified in two independent biological replicates and common peaks. c, Distribution of 9,174 KAP1-ChIP-seq peaks over various DNA elements. d, Distribution of retrotransposon classes among KAP1-ChIP peaks from hESCs (left) or genome-wide (right). e, KAP1 and H3K4me3 ChIP-seq and RNA-seq coverage tracks for a representative region on human chromosome 11 in hESCs (white- or grey-shaded) and TC11-mESCs (yellow-shaded). Blue arrows, derepressed retrotransposons; black arrows, re-activated transcription; red vertical shading, reactivated SVAs; orange shading, reactivated LTR12C. Blue and tan in RNA-seq tracks indicate positive and negative strand transcripts, respectively. Note that while the majority of SVAs display aberrant H3K4me3 signal, for unclear reasons not all SVAs display aberrant transcription in TC11-mESCs. Rep, biological replicate; sup, supernatant; TSS, transcription start site.

Extended Data Figure 2 Mouse KAP1 associates with mouse-specific retrotransposons in mouse ESCs.

a, Distribution of KAP1-ChIP-Seq reads from mESCs (left) and the mouse genome (right) for retrotransposon families as defined by RepeatMasker ( b, UCSC Browser image displaying ChIP-seq tracks for input (grey shading) and KAP1 (red shading) as well as gene annotation and repeat element tracks for a region on mouse chromosome 1. Blue shading, KAP1-positive active mouse L1-subtypes45; purple shading, KAP1-positive active intracisternal A-particle (IAP) retrotransposons. LINES, long interspersed nuclear elements; LTR, long terminal repeat; MMERVK10C, mouse endogenous retrovirus subtype K10C; RMER, medium reiteration frequency repetitive sequence; SINES, short interspersed nuclear elements; TEs, transposable elements.

Extended Data Figure 3 Selection of primate-specific KZNF genes with high expression in hESCs.

a, Schematic of primate-specific KRAB zinc-finger genes subdivided in different clades based on previous analysis7. KZNFs shown in b are highlighted in red. b, DESeq-calculated gene expression levels for the 17 highest expressed KRAB zinc-finger genes in hESCs (dark blue) and macaque ESCs (light blue), subdivided by clades.

Extended Data Figure 4 The SVA VNTR domain is necessary and sufficient for ZNF91-mediated repression of luciferase activity.

a–c, Schematic of SV40–luciferase constructs used (left) and relative luciferase activity after transfection of the indicated constructs in mESCs (right). a, SVA and SINE-R are strong enhancers (n = 6 biological replicates). b, Deletion analysis reveals the VNTR of SVA is required for ZNF91-mediated reporter regulation. Luciferase activity in the presence of ZNF91 expressed as a ratio of that observed for empty vector with the same reporter. Biological replicates: no VNTR, n = 9; partial VNTR, n = 3; no hex/Alu, n = 2; no hex, n = 2; full length SVA, n = 15; SINE-R, n = 3. Empty vector is set to 100% for comparison. c, 1.5 VNTR repeats are sufficient to confer ZNF91-mediated regulation on an OCT4Enh–SV40–luciferase-reporter. n = 3 biological replicates. **P < 0.01; error bars are s.e.m.

Extended Data Figure 5 SVA is specifically repressed in vivo by ZNF91.

a, b, Normalized DESeq basemean values for H3K4me3 ChIP-seq (a) and RNA-seq (b) for retrotransposon classes that showed a significant change in ZNF91-transfected TC11-mESCs relative to empty vector. SVAs were the only transposable elements that showed a significant decrease in H3K4me3 and RNA-seq values. **Benjamini–Hochberg adjusted-P < 0.01. c, UCSC browser images for a representative SVA element, promoter and L1PA4 element, showing H3K4me3 ChIP-seq signal for hESCs (grey), TC11-mESCs transfected with empty vector (yellow), pools of primate-specific KRAB zinc-fingers (green) and ZNF91 (red). TSSC4: tumor-suppressing subtransferable candidate 4.

Extended Data Figure 6 Evolutionary history of ZNF91.

a, The phylogenetic tree used in multiple sequence alignment and ancestral reconstruction of ZNF91 (Supplementary Information File 3). ‘hu 1.1’, ‘ch 1.1’ and ‘go 1.1’ represent human, chimpanzee and gorilla domain 6, respectively, ‘hu 1.2’, ‘ch 1.2’, ‘go 1.2’ represent human, chimpanzee and gorilla domains 7–12, respectively, and ‘hu 2’, ‘ch 2’ and ‘go 2’ represent the ZNF91 sequence from start to domain 5, a breakpoint, and from domain 13 to the end (see Methods). Ancestors are labelled with first letters of leaf species below them, for example, HCG is a human–chimp–gorilla ancestor. b, Immunoblot incubated with anti-HA antibody on lysates of HEK293FT cells transfected with HA-tagged human, great ape, hominine and macaque ZNF91 proteins or lysates transfected with an empty vector and pCAG–GFP. Asterisks denote reconstructed ancestral proteins. c, ZNF91 domain deletion analysis showing relative luciferase activities on the SVA-D–SV40 luciferase reporter after transfection of empty vector or ZNF91 deletion constructs in mESCs. Error bars are standard deviation. Numbers in parenthesis indicate zinc-fingers present in the ZNF91 deletion construct. *P < 0.05; **P < 0.01. Biological replicates: empty vector, n = 42; ZNF91 (1–11), n = 4; ZNF91 (1–24), n = 7; ZNF91 (1–30), n = 4; ZNF91 (1, 2, 23–36), n = 3.

Extended Data Figure 7 L1PA4 elements are repressed by primate-specific ZNF93.

a, Relative luciferase activity on a L1PA4– and a OCT4-enhancer–SV40–luciferase-reporter after transfection of 14 KZNFs in mESCs. Significance measured relative to empty vector. n = 3 biological replicates; *P < 0.05; **P < 0.01; error bars are s.e.m. b, Immunoblot showing that ChIP with antibody ab104878 predominantly reacts with a protein of 70 kDa (left panel) and co-immunoprecipitates KAP1 (right panel). HC, heavy chain of IgG. c, Immunoblot demonstrating that ChIP with ab104878 detects overexpressed ZNF93 in 46c mESCs as a 70 kDa protein. d, Repeat Browser (see Methods) displaying ChIP-seq coverage tracks for ab104878 (ZNF93; yellow shading) and KAP1 (blue shading) for a selection of KAP1-bound retrotransposons. e, ChIP-qPCR for amplicons in L1PA4 and LTR12C elements on chromosome 11 in TC11-mESCs after transfection with an empty vector or ZNF93 and ChIP with ab104878. ChIP enrichment is plotted as percentage of input. n = 3 biological replicates; *P < 0.05; error bars are s.e.m.

Extended Data Figure 8 Reconstruction of the evolutionary history of ZNF93.

a, Schematic based on the multiple sequence alignment of ZNF93 orthologues (Supplementary Information File 4). Red shaded area, deletion of zinc-fingers; green shaded area, gain of zinc-fingers; green stripes, gained zinc-fingers; dark blue stripes, zinc-fingers that changed contact residues in the lineage to humans; light blue stripes, changes in other lineages; brown stripes, zinc-fingers with different binding residues between macaques and gibbons, with gibbons sharing the great ape conformation. For this last group of zinc-fingers, it is unknown (represented with a ? symbol) whether the change happened in monkeys or in the LCA of gibbons and great apes after the divergence of Old-World monkeys (see Methods). Asterisks denote reconstructed ancestral proteins. b, Relative OCT4-enhancer–SV40p–luciferase activity for reporters with the indicated L1PA4-derived sequences after co-transfection of an empty vector or various ZNF93 constructs. **P < 0.01; error bars are s.e.m.

Extended Data Figure 9 Schematic of L1Hs retrotranspostion assay.

a, Schematic of constructs tested indicating the site of 129L1PA4 transplant into L1Hs and concept of L1–GFP assay24 in which GFP expression marks cells where a transfected L1 episome has retrotransposed into a HEK293 cell’s chromosomes. ORF, open reading frame; CMV, cytomegalovirus promoter; SD, splice donor; SA, splice acceptor; PvuII, restriction enzyme site.

Extended Data Figure 10 Evolutionary history of L1PA3-6030, L1PA3-6160 and the VNTR size in SVA.

a, Phylogenetic tree, rooted on L1PA4, generated using the Minimum Evolution method42 for fifty 3′-end sequences of L1PA3-6030 and L1PA3-6160, and three 3′-end sequences for L1PA2 and L1PA4. b, Bar graphs showing the number of SVA-_A through SVA_F insertions in each great ape genome. c, Distribution of VNTR size for untruncated SVA elements in the human genome plotted for each SVA-subfamily. The number of untruncated elements identified for each subtype is indicated.

Supplementary information

Supplementary Information 1

This file contains construction details and associated primers and gene sequences for the plasmids used in this study. (PDF 238 kb)

Supplementary Information 2

This file contains primers used for generating sequence data to fill in genome assembly gaps around ZNF91 and ZNF93 in various primate genomes. (PDF 60 kb)

Supplementary Information 3

This file contains full multiple sequence alignment for ZNF91. (PDF 435 kb)

Supplementary Information 4

This file contains full multiple sequence alignment for ZNF93. (PDF 195 kb)

PowerPoint slides

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Jacobs, F., Greenberg, D., Nguyen, N. et al. An evolutionary arms race between KRAB zinc-finger genes ZNF91/93 and SVA/L1 retrotransposons. Nature 516, 242–245 (2014).

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI:

This article is cited by


By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.


Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing