The peer review process is often seen as something that ends at the point of publication. But it is only after publication that most conversations surrounding a paper can begin! By virtue of an extended audience, often the feedback one receives at this post-publication stage is just as valuable as the feedback received during the initial peer review process. This was perhaps best-emphasized to me following a recent publication on antimicrobial peptide evolution in Diptera. Our reviewers for this publication were experts in insect immunity and symbiosis, and contributed valuable input to improve the manuscript as a whole. However it was only after presenting this work to a diverse audience that key questions regarding some elements of the story were asked. Herein I summarize these key questions raised, and provide answers that hopefully further improve the reader's confidence in the claims made in the publication: Hanson MA, Lemaitre B, Unckless RL. 2019. Dynamic Evolution of Antimicrobial Peptides Underscores Trade-Offs Between Immunity and Ecological Fitness. Frontiers in Immunology, 10, 2620. https://doi.org/10.3389/fimmu.2019.02620 The views expressed here in this post-publication discussion are solely those of myself (Mark Hanson). Summary The following commentary responds to constructive criticisms raised by respected colleagues post-publication. The conclusions of the manuscript are (in my opinion) broadly strengthened by incorporating and responding to the comments raised. This includes 1) a semantic correction of interpretation regarding the “sterile ecology” argument, focusing instead on evolving towards “specialized ecology,” 2) a more robust analysis of correlation regarding AMP evolutionary patterns, and 3) the inclusion of the plant-parasitic Scaptomyza flava, a Drosophilid that has independently evolved herbivory ~20mya, and has also reduced AMP copy number relative to its closest outgroup D. grimshawi. This pattern of copy number reduction is similar to how D. sechellia (which feeds exclusively on toxic morinda fruit) has reduced Attacin copy number relative to its sister lineage D. melanogaster, and supports the notion that specialization of ecological niche (such as herbivory) is associated with AMP loss. The discussion here is only intended to supplement the published manuscript, which is a finished product where the data presented within are already sufficient to support the major claims on observed trends in AMP evolution. Introduction to comments on feedback received Following the publication "Dynamic Evolution of Antimicrobial Peptides Underscores Trade-Offs Between Immunity and Ecological Fitness" I received various pieces of constructive feedback from colleagues that would have improved the paper. While it is regrettably too late to incorporate them into the official publication, this form of post-publication peer review raised points that seemed relevant and useful to address some language concerns of the initial manuscript, affirm existing results, and extend the analysis using a dataset I was not previously aware of. The major reason I have typed up this response is because I was curious of what I would find! Would the conclusions stand up to increased scrutiny? It is always a bit nerve-wracking to put your assumptions/hypotheses to the test, but the more important aspect in science is to ascertain if your results accurately reflect reality. Below are summaries of key questions, and my own responses to these issues raised by colleagues post-publication. Three key comments raised by colleagues post-publication: 1. A “sterile” ecology likely doesn’t exist. This is completely fair. The word sterile is thrown around in this manuscript a lot; probably far more often than it should have been. In cereal weevils, it has been reported (data not shown) that no gut microbes could be detected via PCR or cell imaging [1], so there is certainly a spectrum of microbial colonization amongst ecological niches. Plants of course have a vested interest in preventing pathogenic microbial growth, and this is the logic behind calling live-plant-feeding ecologies sterile: presumably living plant tissue offers a food resource with massively reduced microbial presence, and as a consequence, a corresponding reduction in pathogen pressure. However internal plant tissue is not sterile. Sterile is the absence of all other microbes; a near impossible standard in the wild. For instance, endophytes are microbial symbionts of plant tissue that can be found in the roots or leaves, and live within plant nodules or glands [2]. These bacteria and fungi are present in living plant tissue, and therefore internal plant tissue is not functionally sterile. It is interesting to note that these endophytes display genome reduction characteristics similar to obligate symbionts of insects [2]. It is tempting to speculate that such endophytes are avirulent towards insects, as their metabolic needs are intricately tied to their host plant. The consequence of this logic would presume such endophytes would make poor insect pathogens, but various exceptions could be true (e.g. acting as defensive endosymbionts). However the prior use of the word sterile also does a disservice to the finding that Diptericin B has been lost in two mushroom-feeding Drosophila by independent mutations, and loss of one Attacin in D. sechellia. Instead, the key character that seems to be associated with loss is not sterile ecology, but rather specialized ecology. It seems more universal to report that specialization on certain ecological niches (e.g. living plant tissue, ephemeral mushroom sites) can promote AMP loss. This could be due to reduced benefit for AMPs that defend most prominently against specific pathogens (e.g. Diptericin and Providencia rettgeri), pathogens that may no longer be encountered in the new ecological niche, or an absence of pathogenic microbes more generally. Of course, other selective forces could be at play. 2. Some of the data could be analyzed more robustly. This presents itself in two key aspects of the manuscript: i) The correlation of plant-feeding and AMP loss is reported in Figure 1, but no correlation statistical analysis is presented or even addressed. Of the four lineages with AMP loss observed, all three distinct plant-feeding lineages were included. As there were only three unique plant-feeding lineages screened, probing for statistically significant correlations are likely to violate assumptions of normality. Ignoring this limitation (at my own peril!!!), plant-feeding significantly associates with AMP loss when including only unique non-Drosophila lineages (not counting pseudoreplication of e.g. three Tephritids) (fisher’s p = .003). The output of this analysis is given at the end of this report. We analyzed the speciose Drosophila separately as the quality of sequencing was generally better, and we were capable of recovering exact genomic loci. We could therefore better determine copy number variation beyond the broad categories of AMP family gain/loss, which is also more relevant given the shorter evolutionary timescales at play. ii) Diptericin evolution towards DptB-like sequence in Tephritids and Drosophilids is described as “convergent evolution,” but the cladogram/alignment presented in Figure 2a presents very few lineages to demonstrate this. It is possible that instead the ancestral molecule was DptB-like, and rather the non-fruit-feeding lineages shown (e.g. Glossina morsitans, Ephydra gracilis, Themira minor) all converted their DptB-like genes to some other common sequence. This figure was not designed well to highlight commonalities amongst other molecules. However the DptB-like motifs in the highlighted regions are not found in outgroup Diptericins not shown in Figure 2. As an example, the site key for defence is typically a “DXR” in outgroup Diptericins, but consistently “(Q/N)WG” in Tephritid and Drosophilid DptB-like genes; examples of this region in outgroups are included in .fasta format at the end of this post, and a full alignment of Diptericins is available in supplemental data provided on ResearchGate (and I am happy to share further data upon request). 3. Scaptomyza flava Additionally, it was brought to my attention that the genome of Scaptomyza flava was deposited in GenBank independent of a publication (BioProject: PRJNA494789); this Drosophilid fly is a leaf-miner like Liriomyza trifolii, and a member of the paraphyletic Drosophila subgenus [3]. The divergence of plant-feeding lineages in our analysis from their closest relatives all occurred at least ~100mya ([4];Timetree.org); e.g. Rhagoletis and Bactrocera (two fruit-feeding Tephritids) diverged approximately 99mya, and the plant-feeding Tephritids diverged even earlier. However S. flava and Drosophila grimshawi diverged only 30-48mya. Within Drosophila, we were able to determine genomic synteny and accurately compare copy number variation. For instance, D. sechellia has lost one copy of the Attacin gene family, and has a highly specialized ecology feeding on toxic morinda fruit. Likewise D. busckii had a remarkable 9 coding Diptericin genes, and is known to arrive to decomposing organic matter later than D. melanogaster [5]. I screened S. flava for AMP copy number variation relative to its closest relative(s). I found one Defensin gene and one Metchnikowin gene, in agreement with copy numbers in other Drosophila. I found 4 Attacin genes, including one orthologue of AttA/AttB, two orthologues of AttC, and one orthologue of AttD. This same complement of Attacins is found in the closest outgroup D. grimshawi, suggesting no gain or loss in comparisons between these two lineages. Drosocin and Cecropin were difficult to ascertain an expected copy number for: Drosocin copy number varies by outgroup: D. mojavensis (1 gene), D. virilis (2 genes), D. grimshawi (4 genes) [6]. Scaptomyza flava, has 2 Drosocin genes which appear to be coding. Cecropin copy number also varies by outgroup: D. mojavensis (3 genes), D. virilis (4 genes), and D. grimshawi (7 genes). I found four Cecropin genes in one locus in S. flava (comparable locus in D. grimshawi has 5 Cecropins). Intriguingly, one of these four Cecropins has an insertion of ~750bp in exon two, also involving the loss of the terminal stop codon in the displaced part of exon 2 (mutation resulting in non-stop). Thus, this Cecropin gene appears to be non-functional. For Diptericin: I found three Diptericin genes (2 DptC clade, 1 DptB clade) in S. flava syntenic with the three Diptericins of D. grimshawi [6]. One of the two DptC clade Diptericins has three deletions totalling approximately 99 base pairs, as well as numerous premature stop codons in the Diptericin G domain prior to the key functional site highlighted in Unckless et al. [7], suggesting this Diptericin is non-functional. Thus, globally S. flava has pseudogenized one Cecropin gene, though the number of Cecropins in the last common ancestor of D. grimshawi and S. flava is unknown. Scaptomyza has also mutated one copy of Diptericin that is a direct loss compared to its closest outgroup. Overall, S. flava has two AMP mutation events resulting in putative null alleles, which both result in reduced copy number relative to its closest outgroup D. grimshawi. I have included the S. flava AMP pseudogenes in .fasta format at the end of this report. Discussion and conclusion I felt compelled to perform this post-publication reflection as the comments by my colleagues raised key concerns that I felt could be readily addressed. I also don’t see why attempts to improve a paper’s methodology should end after peer review has completed, as if publication is the end of the conversation. The additional analysis and commentary provided here do not change the message of the paper, but they do improve the discussion of its results and the weight of the evidence presented in the manuscript. Hopefully this discussion clarifies what evolutionary forces might be at play in AMP family gain/loss, and the additional sequence comparisons here better demonstrate the evolution of DptB-like genes was "convergent evolution.” The most parsimonious interpretation of the cladogram in Fig. 2a is also convergence, but the context presented there does not demonstrate this as robustly. Excitingly, the additional analysis of the S. flava genome was broadly consistent with the proposed findings that plant-feeding results in loss of AMPs. The Scaptomyza switch to herbivory is projected to have occurred approximately 20mya [3], a relatively recent evolutionary event. If AMPs are indeed deleterious, and selection should act to remove them quickly from the population, should there have been more instances of AMP loss in S. flava? I am unsure of this for the same reasons that AMP mutant generation was difficult in the first place: random mutation is unlikely to target AMP genes as these genes are incredibly short (most are encoded by fewer than 300 nucleotides). Indeed, this is cited as a major reason that AMP mutant analysis was not performed until the advent of specific gene editing via CRISPR/Cas9 [8,9]. In the field, AMP mutation would need to arise by random chance, the mutant individual would need to win the genetic lottery, and the effect would have to be strong enough to overcome genetic drift for the mutation to be inherited in a stable fashion and eventually lead to fixation; while DptA null segregation in wild D. melanogaster suggests loss is not an entirely passive process, AMPs are amongst many aspects that could contribute to organismal fitness. Given the short timeframe since S. flava evolved herbivory (~20mya), pseudogenization of two AMP genes is already quite striking. It should be noted that in all other Drosophila screened, we only saw either no change or net gains in AMP gene copy number (unless specified, as was the case for D. sechellia and also mushroom-feeding flies). Moreover, the two AMP genes pseudogenized in S. flava are both genes that were similarly lost in other plant-feeding lineages (Cecropins in both Mayetiola destructor and Liriomyza trifolii, and Diptericins in both Tephritid plant-parasites and mushroom-feeding Drosophila). Given a fraction of the time that other plant-feeding lineages have had since their divergence, S. flava has already reduced its complement of classic AMP genes by two from a total of 15. Overall, the loss of AMPs in plant-feeding fly lineages appears robust to the inclusion of an additional herbivorous fly, S. flava, in the analysis. References: 1. Heddi A, Zaidman-Rémy A: Endosymbiosis as a source of immune innovation. Comptes Rendus - Biol 2018, 341:290–296. 2. Pinto-Carbó M, Gademann K, Eberl L, Carlier A: Leaf nodule symbiosis: function and transmission of obligate bacterial endophytes. Curr Opin Plant Biol 2018, doi:10.1016/j.pbi.2018.01.001. 3. Goldman-Huertas B, Mitchell RF, Lapoint RT, Faucher CP, Hildebrand JG, Whiteman NK: Evolution of herbivory in Drosophilidae linked to loss of behaviors, antennal responses, odorant receptors, and ancestral diet. Proc Natl Acad Sci U S A 2015, doi:10.1073/pnas.1424656112. 4. Kumar S, Stecher G, Suleski M, Hedges SB: TimeTree: A Resource for Timelines, Timetrees, and Divergence Times. Mol Biol Evol 2017, 34:1812–1819. 5. Markow TA: The natural history of model organisms: the secret lives of Drosophila flies. Elife 2015, 4:e06793. 6. Hanson MA, Hamilton PT, Perlman SJ: Immune genes and divergent antimicrobial peptides in flies of the subgenus Drosophila. BMC Evol Biol 2016, 16:228. 7. Unckless RL, Howick VM, Lazzaro BP: Convergent Balancing Selection on an Antimicrobial Peptide in Drosophila. Curr Biol 2016, 26:257–262. 8. Lemaitre B, Hoffmann J: The Host Defense of Drosophila Melanogaster. Annu Rev Immunol 2007, 25:697–743. 9. Hanson MA, Dostálová A, Ceroni C, Poidevin M, Kondo S, Lemaitre B: Synergy and remarkable specificity of antimicrobial peptides in vivo using a systematic knockout approach. Elife 2019, 8. Fisher’s association test for ecology: Thanks to user “StupidWolf” on stackoverflow for their aid in this analysis: https://stackoverflow.com/questions/58903067/correlation-of-categorical-data-to-binomial-response-in-r#58903796 Generate the data frame in R (should probably use data.frame…): species<-c("Aaeg","Mcin","Ctri","Crip","Calb","Tole","Cfus","Mdes","Hill","Cpat","Mabd","Edim","Tdal","Tmin","Edia","Asus","Ltri","Gmor","Sbul","Cvic","Egra","Pvar") scavenge<-c(1,1,0,1,1,1,1,0,1,0,1,1,1,0,0,1,0,0,0,0,1,1) dung<-c(0,0,0,0,0,0,1,0,1,0,0,0,0,1,0,0,0,0,1,1,0,0) pred<-c(0,1,1,1,1,0,0,0,0,1,0,0,0,0,0,0,0,0,1,1,0,0) nectar<-c(1,0,0,0,0,0,0,0,1,0,0,1,0,0,0,0,0,0,1,1,0,0) plant<-c(0,0,0,0,0,0,0,1,0,0,0,0,0,0,1,0,1,0,0,0,0,0) blood<-c(1,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,1,0,0,0,0) mushroom<-c(0,0,0,0,0,0,1,0,0,0,1,0,0,0,0,0,0,0,0,0,0,0) loss<-c(0,0,0,0,0,0,1,1,0,0,0,0,0,0,1,0,1,0,0,0,0,0) #1 means yes, 0 means no data<-cbind(species,scavenge,dung,pred,nectar,plant,blood,mushroom,loss) data #check data table #Perform fisher’s test library(dplyr) library(purrr) # function for the fisher test FISHER <- function(x,y){ FT = fisher.test(table(x,y)) data.frame( pvalue=FT$p.value, oddsratio=as.numeric(FT$estimate), lower_limit_OR = FT$conf.int[1], upper_limit_OR = FT$conf.int[2] ) } # define variables to test FEEDING <- c("scavenge","dung","pred","nectar","plant","blood","mushroom") # we loop through and test association between each variable and "loss" results <- data[,FEEDING] %>% map_dfr(FISHER,y=data$loss) %>% add_column(var=FEEDING,.before=1) #Odds ratios for different variables correlating with plant feeding > results var pvalue oddsratio lower_limit_OR upper_limit_OR 1 scavenge 0.264251538 0.1817465 0.002943469 2.817560 2 dung 1.000000000 1.1582683 0.017827686 20.132849 3 pred 0.263157895 0.0000000 0.000000000 3.189217 4 nectar 0.535201640 0.0000000 0.000000000 5.503659 5 plant 0.002597403 Inf 2.780171314 Inf 6 blood 1.000000000 0.0000000 0.000000000 26.102285 7 mushroom 0.337662338 5.0498688 0.054241930 467.892765 Plant association with AMP family loss: fisher’s p = .002597403, though the odds ratio approaches infinity. This analysis isn't appropriate for publication, but it is good to confirm the results trend towards statistical significance.
Fasta of Diptericin G domains highlighting the site key for defence against P. rettgeri: Fasta, with samples of the “DXR” or “(Q/N)WG” polymorphic residue highlighted in red. Tephritid and Drosophilid DptB-like genes are bolded. Mayetiola destructor Diptericin clusters via long-branch attraction to Diptericins of Drosophila [6], and also encodes a serine at this site similar to the Drosophila DptA/DptC clades. Also included are newly analyzed DptC and DptB gene sequences from S. flava, and I will note that the 2-exon DptB is the ancestral gene giving rise to the 1-exon Drosophila DptA/DptC clade via an ancestral RNA-mediated duplication event [6]. For species relatedness see Hanson et al. (2019; Frontiers in Immunology) Figure 1. The gene structure at this C-terminal motif is consistently “DXR” in outgroup flies, but “(Q/N)WG” in DptB-like sequences. >Mayetiola_destructor_Dpt-partial GGPYGNSRPSYGGGVSYTHRF >Sphyracephala_brevicornis_Dpt-partial GGPYGNSRPDFRGGAVYTFRF >Megaselia_abdita_Dpt-partial GSKWGSSPTDRRVGGQYTYRF >Themira_minor_Dpt-partial GGPWGNSKPDYRVGGVYTFRF >Bactrocera_dorsalis-Tephritid_DptB-like-partial GGRYGNSPPNWGVGGQYTFRF >Glossina_morsitans_Dpt-partial GGPYGNSRPDFRGGASYTYRF >Ephydra_gracilis_Dpt-partial GGPYGNSPADYRGGASYTFRF >Drosophila_melanogaster_DptB-partial GGPYGNSRPQWGAGGVYTFRF >Scaptomyza_flava_DptB-partial GGPYGNSRPNWGAGAAYTFRF >Scaptomyza_flava_DptC1_pseudogene-partial GGPYGDSKPS*GYGGNYRFRF >Scaptomyza_flava_DptC2-partial GGPYGDSKPSYGFGGNYRFRF FASTA of S. flava Dpt and Cec AMPs and pseudogenes >Scaptomyza_flava_DptB_CDS ATGCAACTTAGTCTGGGTTTACTGCTGTTCCTCGGCTTGAACGCCTGCATCTGGGCTTATCCAAATCCTCAGTTTGCTATCCCTGACTTGGCCAACTATGAGACACTATTGCTGGCGGAAAGTTATGATTGGGCGTCTAGTGAAGATGAGGAGCTGCAGCATCGCGTGCGTCGCCAGCTAAACATTCAGGGTGGTGGCAGTCCTCGACAAGGATTCGATCTAAGCGTCAATGGACGTGCACCTGTGTGGCAGAGTGCCAATGGCAGGCATTCCCTAGATGCCACTGGACAATATTCACAGCATCTAGGCGGTCCATATGGCAACAGTCGACCTAATTGGGGAGCTGGTGCAGCTTACACATTCCGATTCTAG >Scaptomyza_flava_DptC2 ATGCAGGTTACATACATTGCCCTATTCTGTTGCCTTGTTGGCTCTGTACTTGCTTTTCCCAATCCCAATCCGGAAGAGCAGAAGGATGTTTGGACTGAGCGCAAACAATATAATCCACCAAATGAGCAACGTTTCTTAGCCGATGGTGGCTACAACAAGGATAAGAGTGGCAAGGATGTGTGGGCTCAAGTACAGGTGCCCGTTTATACCAGCGATAACAAACGTCACGAGTTCGATGTGGTCGGAAAGTATGGACAGCATTTGGGTGGACCTTATGGCGACAGCAAACCCTCTTACGGTTTTGGCGGCAACTACAGATTCCGTTTTTAA >Scaptomyza_flava_DptC1_pseudogene ATGCAGGTTACAATCATTGCTCTATTCTGTTGCTTTGCTTTTCCCAATCCCAATCCGGAAGAGCAGAAGGATGTTTGGACTGAGCGCAAACAATATAATCCTCCAAATGGCAAGGATGTGTGGGCTTAGGTACAGGTGCCCGTCGGAAGATATGGATAGCATTTGGGTGGACCTTATGGCGATAGCAAACCCTCTTAAGGTTATGGAGGCAACTACAGATTTCGTTTTTAA Premature stops in the 1-exon Diptericin C pseudogene are highlighted. >Sfla\Cec1_Scaptomyza flava isolate OHI-9 scaffold00463, whole genome shotgun sequence ATGAACTTCTACAAGATCTTCGTCTTTGTCGCTCTCATCCTTGCCATCAGCTTTGGTCAATCCGAGGCTGGTTGGTTGAAGAAGATTGGCAAGAAAATTGTAAGTCCTTTGAAGGTTATTGCATTCTATAATATATTGATGATAAATTTGTTTTCATAGGAACGCATTGGCCAGCATACTCGGGATGCCACTATCCAAGGATTGGGTGTAGCTCAACAGGCCGCCAATGTTGCTGCAACAGCCAGAGGCTAA >Sfla\Cec2_Scaptomyza flava isolate OHI-9 scaffold00463, whole genome shotgun sequence ATGAACTTCTACAAGATCTTCGTTTTTGTGGCTCTCATCCTTGCCATCAGCATTGGTCAATCCGAGGCTGGTTGGTTGAAGAAGATTGGCAAGAAAATTGTAAGTTCTTTCATAATTTCAAGAAGTTATCGATTAGCTAATAATATTAATTAATCTAGGAACGCATCGGCCAGCACACTCGAGACGCCACCATCCAAGGATTGGGTGTTGCCCAACAGGCCGCCAATGTTGCAGCTACAGCCAGGGGCTAA >Sfla\Cec3_Scaptomyza flava isolate OHI-9 scaffold00463, whole genome shotgun sequence ATGAACTTCTACAAGATCTTCGTCTTTGTTGCTCTTATCCTGGCCATCAGCATTGGTCAATCCGAGGCTGGTTGGTTGAAGAAAATTGGCAAGAAAATTGTAAGTTCTCACAAGCTAAAGCATTTTAAACATATACTAATAACTAGTTTGTCCTTATAGGAACGCATTGGTCAACACACTCGGGATGCCACCATTCAAGGATTGGGTGTCGCCCAGCAGGCCGCCAATGTTGCAGCTACAGCCAGAGGATGA >Scaptomyza_flava_Cec4_pseudogene ATGAACTTCTACAAGATTTTCATTTTTGTTGCCTTTCTCTTGGCCATCGCCATTGGTCAGTCCGAGGCGGGTTGGCTAAAAAAGACTGCTAAGAAAGTTGTAAGTTTTTATAGTTAAAAAAAAATACTAACATTGCATTATAATAAAAAAAATATCCTTTTAGGGAAACACAGTCAAAAAGACAGTGAAAGACGGTGTTCCGGTAGCTCTTGGAACAGCTGCTATACAATCGTTGGGATAATCATCTAACGAAATATTTATAAATCATTTTTTTTTTTTTTTTTTACTTTGCCTATGCTAGCATTTGTATTTCTGTTTCTGTTGTATTTGTCTGTGTTTTTGTTTTGAATTTGGCTCTAGCTCAGTTTGAGTTCTTTTTTTACTTTTTTTTACTCTTCGTTTTTTCAAAAGTTTTTTATCGACGATATTCTTTTTTTTTTTCCCACCAACCAAGTTGTTGGTTTTTTATTCGTCGATTTTTTCTTAATAAAAGGTGTTCTTCTTTTTCTTTTCTGTTCTCTCCAGTTTGGTTTTCGCTTCGTTTTTTTTTTTTTAAATTTCCCCTTCGTTTCTTGTCTTTTATTTTAGTGGGATGTGTTTTGTTTTTGTCTTCTTCGCCTCGTTTCGTTGAGTTGTGGTATCGCCGTTGCATTGTTCGCTGGTCATGTGATGCTCCGCTGCAGTGGCTTAGTTTACTTAGCTTGTCTTTTCTCTTTTCTGTTTATATTCTATTCGTGCATTTCAACTTGAACTTCTCTTCTATCTTCTTTTTTTTTTTTTTTCTCTTTTCCTTGCGCTTTGGTTTGTTCGATGCTGGTTTGTTTGGTTGGATTGGATTGGCAATTGTATTTTCCGTCTCCTGTCTTTATTTTATTTACTTTTTCTTTTCTCTTATCTTTGTTTTTTTTTTGTCGGATTGGTTTGGACACTCGAGTTGCGATGCTTCCGTTCTTGGGTTTTGTCTTGCCGGCCGGGCCTGTTGTGTTGCCGGCCCGGGGATGGGTTGCTT The classic Cecropin terminus including the “ARG*” terminal motif is highlighted, which now codes “ARGW” in the Sfla\Cec4 pseudogene. Comments are closed.
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