SEARCH · Search PubMed

Results for “parasite genetic background”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMed2026

Functional validation of the Plasmodium falciparum K13 C580Y mutation in recently collected Ethiopian isolates.

Recent genomic investigation in Ethiopia identified the first detection of the Plasmodium falciparum Kelch13 (K13) C580Y substitution in the Horn of Africa. To assess its functional impact, we introduced C580Y into two recently collected Ethiopian clinical isolates using CRISPR-Cas9 genome editing. Ring-stage survival assays showed significantly elevated in vitro dihydroartemisinin survival in edited parasites relative to isogenic controls, demonstrating that C580Y confers artemisinin tolerance in contemporary Ethiopian parasite genetic backgrounds.

CRISPR-Cas9↗

PubMed1992

Regulation of immunity to parasites by T cells and T cell-derived cytokines.

Parasitic protozoa and helminths are a diverse group of organisms which together form a major cause of infectious disease in humans and livestock. Studies in animal models have revealed that T lymphocytes and the cytokines they produce play a crucial role in determining the outcome of parasitic infection in terms of both protective immunity and immunopathology. Of particular interest is recent evidence that different parasitic infections in the context of different host genetic background can trigger polarized CD4+ T cell subset responses. The set of cytokines produced by these different T helper responses, in turn, can have opposing effects on the parasite, resulting in either control of infection or promotion of disease. Moreover, cytokines produced by one CD4+ subset can block either the production and/or activity of the cytokines produced by the other subset. The establishment of this state of cross-regulation may be important for parasite survival. CD8+ T cells also appear to play a dual effector/regulatory role in parasite immunity and immunopathology, although the mechanisms underlying their induction and function are less well understood. CD(8+)-mediated cytolytic killing functions have now been demonstrated against a number of different intracellular protozoa, although IFN-gamma produced by the same effector cells may also be critical in host community. In addition to providing highly relevant models for studying the selection and immunobiologic function of T-cell subsets, research on T lymphocyte-parasite interactions is crucial for the design of effective vaccines and immunotherapies and thus has broad practical as well as theoretical ramifications.

Animals↗

PubMed2026

Identification of lineage-associated polymorphisms in the ROP18 3' flanking region and development of molecular assays for differentiation of Toxoplasma gondii lineages.

BACKGROUND: Toxoplasma gondii (T. gondii) exhibits substantial genetic diversity, and different parasite lineages are associated with distinct epidemiological distributions and biological characteristics. Accurate molecular characterization of T. gondii strains is important for understanding parasite population structure and transmission patterns. However, existing genotyping approaches often require multiple loci, extensive experimental procedures, or complex data analysis. Therefore, simplified and reliable molecular markers for rapid lineage differentiation are still needed. METHODS: In this study, comparative genomic analysis was performed using representative T. gondii strains with well-defined genetic backgrounds and virulence phenotypes. The ROP18 genomic region, including partial genomic sequences, 5' flanking regions, coding sequence (CDS), and 3' flanking regions, was analyzed to identify informative polymorphic signatures. A short conserved sequence region containing lineage-associated polymorphic sites was identified within the ROP18 3' flanking region. Based on these sequence signatures, HRM-PCR and TaqMan MGB probe-based real-time PCR assays were developed and evaluated using plasmid standards and representative T. gondii genomic DNA samples. RESULTS: Phylogenetic analyses based on different ROP18 genomic regions demonstrated distinct clustering patterns among analyzed strains. Although the ROP18 3' flanking region was highly conserved, a short conserved sequence region containing informative polymorphic sites was identified, and the combination of these sites generated three distinct lineage-associated ROP18 patterns. Analysis of publicly available genomic datasets further demonstrated that individual strains contained one of these defined patterns rather than multiple patterns simultaneously. The developed HRM-PCR assay successfully discriminated the three ROP18-associated patterns based on distinct melting profiles with good reproducibility. Furthermore, the TaqMan MGB probe-based assay enabled specific identification of different ROP18-associated patterns through defined probe-recognition combinations and showed good analytical performance. CONCLUSION: This study identifies novel lineage-associated molecular signatures within the ROP18 3' flanking region and establishes complementary HRM-PCR and TaqMan MGB probe-based approaches for rapid molecular differentiation of T. gondii strains. These findings highlight the potential of conserved non-coding regions adjacent to functionally important genes as informative targets for parasite genotyping and provide a practical complementary tool for epidemiological surveillance and strain characterization.

HRM-PCR↗

PubMed1992

Leishmania amazonensis infection: a comparison of in vivo leishmanicidal mechanisms between immunized and naive infected BALB/c mice.

In vitro studies have shown that both macrophage activation and destruction of parasitized macrophages lead to leishmania destruction. The relative role played by such mechanisms in vivo have not been properly evaluated. We took advantage of the model of intravenous immunization with solubilized leishmanial antigen which renders partially resistant the otherwise highly susceptible BALB/c mice to address this issue avoiding the interference of different genetic backgrounds. Leishmania destruction occurred in three situations: destruction of the parasitized macrophage, which were in close contact with lymphocytes or eosinophils; extracellular damage, always surrounded by small foci of granulocytes; and parasite damage inside activated macrophages. Destruction of the parasitized macrophages was frequently seen in immunized and protected animals. Our observations suggest that destruction of parasite-loaded macrophages is an important mechanism of host protection in experimental cutaneous leishmaniasis.

Animals↗

PubMed2025

Acetyl-CoA synthetase mutations affect the susceptibility of Plasmodium falciparum to antimalarial drugs.

Plasmodium falciparum acetyl-CoA synthetase (PfAcAS) is an important source of acetyl-CoA. We detected mutations S868G and V950I in PfAcAS by whole-genome sequencing analysis in certain recrudescent parasites after treatment with artesunate and dihydroartemisinin-piperaquine. Using CRISPR/Cas9 technology, we engineered parasite lines to carry the PfAcAS S868G and V950I mutations in two genetic backgrounds and evaluated their susceptibilities to antimalarial drugs in vitro. The results demonstrated that PfAcAS S868G and V950I mutations alone or in combination affected the susceptibility of P. falciparum to several antimalarial drugs, including the artemisinin derivatives (dihydroartemisinin, artesunate, and artemether) and chloroquine, although absolute changes in susceptibilities were modest.IMPORTANCEMalaria, an infectious disease caused by Plasmodium parasites and transmitted by mosquitoes, continues to be one of the most pressing public health challenges worldwide. P. falciparum has demonstrated reduced sensitivity to artemisinin-based combination therapies (ACTs), thereby intensifying the difficulties associated with malaria management. Currently, only a limited number of molecular markers exist for identifying drug resistance in P. falciparum, and these markers do not fully elucidate the mechanisms behind this resistance. In this study, we performed whole-genome sequencing analysis on P. falciparum strains that reemerged following ACT treatment. We aim to identify molecules potentially associated with drug resistance, which may provide new molecular markers for monitoring drug resistance in P. falciparum.

Plasmodium falciparum↗

PubMed1988

Nematospiroides dubius: two H-2-linked genes influence levels of resistance to infection in mice.

Strains of mice sharing common H-2 haplotypes but different genetic backgrounds, and H-2 congenic strains of mice differing only at H-2 genes were studied to assess the role of H-2 and non-H-2 genes in immunity to challenge infections with the nematode parasite Nematospiroides dubius. Strains of mice sharing the H-2k haplotype were uniformly more susceptible to challenge than strains expressing H-2q alleles, regardless of genetic background. However, in some cases strains of mice sharing the k or q haplotypes differed significantly in levels of resistance. Therefore, non-H-2 genes must influence the response observed. H-2 cogenic strains of mice differed markedly in their ability to resist challenge infections. Mice sharing the C57BL/10 background but expressing k alleles were very susceptible to challenge, while the H-2q, H-2f, and H-2s, haplotypes were associated with resistance. Studies of H-2 congenic recombinant strains of mice suggested that two H-2 genes influence the antiparasite response. One of these genes maps to the left of E alpha and the other to the D-end of the H-2 complex. It is concluded also that the unique configuration of H-2 genes in F1 hybrids contributes to increased resistance to challange.

Alleles↗

PubMed1988

Schistosoma mansoni: induction of severe glomerulonephritis in female BXSB mice following chronic infection.

C57BL/6 (B6) and female BXSB mice were infected with 10 cercariae of Schistosoma mansoni per head in order to examine whether chronic parasite infection induced glomerulonephritis (GN) with polyclonal B-cell activation. Six months after the infection, mice were sacrificed and various immunological and histopathological examinations were performed. The following results were obtained. (1) Severe GN was induced in parasite-infected female BXSB mice. The renal changes were similar to those of male BXSB mice which spontaneously develop lupus-like GN. No substantial renal changes were observed in infected B6 mice. (2) Massive IgG and C3 deposits were found in capillary loops and also at the mesangial area of infected BXSB mice. No significant IC deposits were found in the kidney of infected B6 mice. (3) A high level of IC was detected in sera of some parasite-infected female BXSB mice, though no significant difference in the level of IC was found between infected and control mice. (4) Numbers of spleen IgG-producing cells were significantly increased in infected B6 mice. Infected female BXSB mice with splenomegaly showed higher numbers of IgGPC than uninfected mice, but there was no difference between the groups. These results suggest that genetic backgrounds played an important role in the development of lupus-like GN following the chronic infection of parasite-causing polyclonal B-cell activation.

Animals↗

PubMed1989

Genetic variation in the humoral immune responses of mice to the nematode Trichuris muris.

Genetically based differences in the antibody responses to the large intestinal nematode Trichuris muris were studied in two groups of H-2 congenic strains of mice that differed in their relative resistance to infection with this parasite. The primary antibody response to parasite excretory/secretory (E/S) antigen was predominantly an IgG response with the strains forming two distinct groups, defined by their genetic background. The more susceptible B10 genetic background mice had strikingly higher antibody levels than mice of the BALB genetic background. Superimposed upon these background effects were clearly defined influences attributable to H-2-linked genes, strains which differed genetically only at H-2 loci exhibiting differences in the kinetics of the antibody response. Only B10.G and B10.BR mice showed any great increase in IgM levels post-infection. No IgA specific to E/S antigen was detected in the peripheral circulation of any strain at any time post-infection. Antibody responses to a 40-43 kD antigen revealed clear H-2-linked gene effects, with mice sharing the H-2k haplotype (B10.BR, BALB/K) exhibiting considerably higher total antibody levels than strains expressing other haplotypes; mice of the H-2d haplotype (BALB/c, B10.D2/n) responded very weakly to this antigen. A Western blot analysis of antigen recognition by antibody revealed similarities between the mouse strains in their total antibody responses to T. muris E/S antigen. However, immunoprecipitation studies showed that in general the more susceptible B10 congenic strains had wider spectra of antigen recognition than the BALB congenics. Strains sharing the same H-2 haplotype had dissimilar antigen recognition profiles, but strains sharing the H-2b haplotype (B10, BALB/B) recognized a low mol. wt antigen (20-23 kD) not recognized by any other strain, suggesting an exclusively H-2b restriction in the recognition of this antigen. These results support the conclusion that both H-2-linked and background genes play important roles in controlling the humoral immune response to T. muris infection.

Animals↗

PubMed2026

Genetic diversity of Plasmodium falciparum helical interspersed subtelomeric (phistb) gene in Tanzania and neighboring countries.

BACKGROUND: Lysine-rich membrane associated Plasmodium helical interspersed subtelomeric gene (phistb) is a member of the phist family of genes which encodes exported proteins essential for the parasite's survival within infected red blood cells. Recent studies suggest the phistb gene as a promising malaria vaccine candidate, however, its genetic diversity remains understudied. This study assessed the genetic diversity of the phistb gene in regions of varying malaria transmission aiming to generate data and improve our understanding of this promising malaria vaccine candidate gene. METHODS: Genomic data from 1472 Plasmodium falciparum samples from Tanzania, Kenya, Uganda, and Ethiopia were retrieved in variant Calling file format (VCF) format from the MalariaGEN Pf7 database. Variants were filtered to include only biallelic Single Nucleotide Polymorphism (SNPs) with Variant Quality Score Log- Odds (VQSLOD) > 1 and "PASS" status. Genetic diversity, differentiation, and selection signatures were analyzed using population genetics metrics. RESULTS: After filtering, 1312 samples were retained. Wright's inbreeding coefficient (Fws) showed that 875 (66.7%) samples had monoclonal infections, with the highest proportion of monoclonal infections in Ethiopia (95.3%), followed by Tanzania (67.2%), Kenya (65.7%), and Uganda (50%). Among the 875 monoclonal samples, 88 haplotypes were identified, with Hap_1 (renamed PF3D7) and Hap_13 comprising 37.9 and 21.5 of the samples, respectively. Nucleotide and haplotype diversity were relatively higher in Kenya with 0.097, and 0.88 respectively, compared to the other study populations. The overall fixation index (Fst) was < 0.05, and Principal Component Analysis revealed no clear population sub-structure among countries. Negative Tajima's D values in Tanzania, Kenya, and Ethiopia indicated an excess of low-frequency alleles. CONCLUSION: This study reports low genetic diversity of the phistb gene in the four countries despite varying malaria transmission intensities among them, thus making it a suitable candidate gene for malaria vaccine. Further studies should be conducted to assess individual antibodies recognition of the phistb variants and the ability to elicit cross reactivity to further support its potential as a vaccine candidate.

Plasmodium falciparum↗

PubMed1990

[Is there a future for vaccines against gastrointestinal helminths?].

Vaccines against gastro-intestinal helminths have a large market potential, but they also generally have a narrow range of activity. This is a major drawback in the competition with the broad-spectrum anthelmintics and there is still a long way to go before molecular (recombinant) vaccines will appear on the market. Major problems are the induction of protective gut-mucosal immunity with subunit vaccines and the differences in genetic background within host populations, which largely determine the efficacy of vaccination. As yet the changes for vaccines against blood- and tissue parasites, comprising a number of veterinary important protozoa, seem to be better.

Animals↗

PubMed1985

Prophylactic immunization against experimental leishmaniasis. IV. Subcutaneous immunization prevents the induction of protective immunity against fatal Leishmania major infection.

Durable immunity against fatal L. major infection in genetically susceptible mice can be induced by immunization with 150,000-rad irradiated or heat-killed promastigotes administered i.v. or to a lesser extent i.p. Conversely, subcutaneous (s.c.) and intramuscular (i.m.) injections are not only totally ineffective but generally increase susceptibility to and enhance the progression of the disease, leading to earlier mortality. This detrimental effect is particularly evident with lower infecting challenge doses. Disease exacerbation is apparent in mice given 4 X s.c. injections of as few as 2 X 10(4) irradiated promastigotes, but it appears most potent after doses of 2 X 10(7). When mice given 4 X s.c. injections were subsequently immunized i.v. with 2 X 10(7) irradiated promastigotes, they failed to develop any evidence of protection against infection with 2 X 10(5) promastigotes, whereas mice given i.v. immunization alone were strongly protected. Thus, s.c. injections are capable of blocking the prophylactic effect of i.v. immunization with irradiated parasites. This inhibitory effect can be achieved with a single s.c. injection, although rather less potently than with four, and is even effective against four repeated weekly i.v. immunizations. Once induced, the effect persists undiminished after 100 days. A weaker effect is also inducible by s.c. injection given after i.v. immunization. The blocking effect of s.c. injection is not dependent on continuing viability of the promastigotes, as it can be induced equally readily with heat-killed, formalin-fixed, or sonicated parasites. The phenomenon extends to mouse strains genetically resistant as well as susceptible to L. major infection and, in congenic mice of BALB background, is independent of the major histocompatibility (H-2) gene complex.

Animals↗

PubMed1985

Genetics of resistance to the African trypanosomes. V. Qualitative and quantitative differences in interferon production among susceptible and resistant mouse strains.

The induction of interferon (IFN) was examined in different inbred mouse strains infected with Trypanosoma brucei rhodesiense. Relatively susceptible C3HeB/FeJ mice that do not exhibit variant-specific immunity or control parasitemia did not exhibit detectable IFN throughout the infection. Relatively resistant B10.BR mice that exhibit variant-specific immunity and control the first peak of parasitemia exhibited detectable IFN at two intervals. The appearance of IFN in B10.BR serum first coincided with the onset of the parasitemia 4 days after infection and then disappeared; this IFN peak was predominantly IFN-alpha/beta. The second time of appearance coincided with high titers of antibody and remission of the parasitemia. This IFN was predominantly IFN-gamma. Intermediately susceptible CBA/J mice also exhibited two detectable peaks of IFN; the first IFN-alpha/beta peak coincided with the onset of the parasitemia as in B10.BR mice. The second peak of IFN in the serum of CBA mice, however, was delayed in appearance and lower in concentration compared with B10.BR mice. This peak was characterized as being predominantly IFN alpha/beta. BALB/c mice (also intermediately susceptible) did not exhibit a first peak of IFN-alpha/beta production, but the second peak of IFN-alpha/beta production was similar to that seen in CBA mice. In contrast to infected mice, IFN was induced in both susceptible (C3H) and resistant (B10.BR) mice after immunization with glutaraldehyde-fixed trypanosomes or after chemotherapy of infection. We conclude that both the levels of IFN as well as the type of IFN induced during infection with T. b. rhodesiense depend upon the genetic background of the mouse strain infected. The induction of IFN-gamma in mice of the C57BL background may be linked functionally to more effective parasite control and to the presence of an effective immune response to T. b. rhodesiense.

Animals↗

PubMed1992

Human schistosomiasis mansoni: studies on in vitro granuloma modulation.

Infection with Schistosoma mansoni induces humoral and T cell mediated responses and leads to a delayed hypersensitivity that results in granulomatous inflammatory disease around the parasite eggs. Regulation of these responses resulting in a reduction in this anti-egg inflammatory disease is apparently determined by idiotypic repertoires of the patient, associated with genetic background and multiple external factors. We have previously reported on idiotype/anti-idiotype-receptor interactions in clinical human schistosomiasis. These findings support a hypothesis that anti-SEA cross-reactive idiotypes develop in some patients during the course of a chronic infection and participate in regulation of anti-SEA cellular immune responses. We report here on experiments which extend those observations to the regulation of granulomatous hypersensitivity measured by an in vitro granuloma model. T cells from chronic intestinal schistosomiasis patients were stimulated in vitro with anti-SEA idiotypes and assayed in an autologous in vitro granuloma assay for modulation of granuloma formation. These anti-SEA idiotype reactive T cells were capable of regulating autologous in vitro granuloma formation. Both CD4 and CD8 T cells could be activated to regulate granuloma formation. This regulatory activity, initiated with stimulatory anti-SEA idiotypic antibodies, was antigenically specific and was dependent on the presence of intact (F(ab')2) immunoglobulin molecules. The ability to elicit this regulatory activity appears to be dose dependent and is more easily demonstrated in chronically infected intestinal patients or SEA sensitized individuals.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Helminth↗

PubMedDate not supplied

Immune resistance to Trypanosoma cruzi: synergy of specific antibodies and recombinant interferon gamma in vivo.

The protective effects of interferon gamma (IFN-gamma) against infection by Trypanosoma cruzi were studied in vitro and in vivo in a murine model of infection. The possible synergy between IFN-gamma and trypomastigote-specific antibodies in the rejection of the parasite was also considered. Our results in vitro indicate that IFN-gamma activates macrophages to reject the parasite and this mechanism may lead to a decrease in parasitaemia in vivo. Finally, IFN production in vivo after infection by T. cruzi was compared among mice from different genetic backgrounds. Reduced parasitaemia and extended survival correlated with the early production of circulating IFN-gamma and anti-trypomastigote antibodies after infection. The appearance of an unusual type of circulating IFN in response to infection by T. cruzi was also detected; this IFN was resistant to neutralization by antibodies to IFN-alpha/beta and to IFN-gamma.

Animals↗

PubMed1990

The influence of genes mapping within the major histocompatibility complex on resistance to Trichuris muris infections in mice.

Two panels of H-2 recombinant strains of mice were used in an attempt to map the H-2-linked genes which control resistance to infection with Trichuris muris. Response phenotypes could be related to the presence of 'resistance' (q,b) or 'susceptibility' (k,d) alleles at I-A. The influence of these genes was modulated by other alleles, particularly q or d alleles, at the D end of the H-2. Absence of I-E molecules correlated with resistance to infection in some but not all strains studied. Thus the (B10.BR x B10.G) F1 strain which expressed I-Ek gene products was resistant to infection. A study of the time-course of infection in strains of mice expressing q alleles throughout the H-2 on 4 different genetic backgrounds (NIH, SWR, DBA and B10) revealed that most strains were resistant to infection. However, the DBA/1 strain exhibited differential responsiveness, 4 out of 6 individuals harbouring mature adult parasites on day 35 post-infection.

Alleles↗

PubMed1987

Histopathologic changes induced by vaccination in experimental cutaneous leishmaniasis of BALB/c mice.

Highly susceptible BALB/c mice became partially resistant to Leishmania mexicana amazonensis infection after intravenous immunization with solubilized homologous promastigote antigen. Immunized BALB/c mice exhibited mixed mononuclear cell reactions, with granulomatous inflammation, collagen deposition, and fibrinoid necrosis at the site of infection. In contrast, naive animals displayed a monomorphic picture composed of largely vacuolated and parasitized macrophages with areas of coagulative necrosis. Electron microscopy revealed an increased number of eosinophils, sometimes in close contact with parasitized macrophages, in immunized animals. These findings illustrate that histologic changes reflect host immune status in cutaneous leishmaniasis, and that susceptibility of BALB/c mice to L m amazonensis, although dependent on genetic background, can be artificially modified.

Animals↗

PubMed1988

Immunoregulation in murine malaria. Susceptibility of inbred mice to infection with Plasmodium yoelii depends on the dynamic interplay of host and parasite genes.

Inbred and H-2 congenic mouse strains were tested for their ability to resist infections with the non-lethal 17X or with the lethal YM isolates of Plasmodium yoelii. DBA/2 and B10.D2 mice, which best resisted infections with non-lethal P. yoelii, were exquisitely susceptible to infection with lethal isolates of this malaria species. In contrast, B6 and B10 mice, which were susceptible to infection with non-lethal P. yoelii, were resistant to infection with the lethal isolates. This reversal of host response phenotype was influenced by H-2 genes, as evidenced by the divergent responses of the H-2 congenic strains B10 and B10.D2. However, a survey of mouse strains sharing common H-2 genes, but expressing different genetic backgrounds, demonstrated that genes outside the H-2 complex also influence the outcome of P. yoelii infections. By enumerating the numbers of P. yoelii-specific antibody-secreting cells in the spleens of infected mice, it was demonstrated that B6 mice, although susceptible to infection with non-lethal P. yoelii, nonetheless made a far stronger anti-parasite response after infection than did resistant DBA/2 mice. Using FACS analysis it was shown that infected B6 mice also produced large amounts of antibodies which bound to the surface of uninfected RBC. Thus, in B6 mice infected with non-lethal P. yoelii, a strong parasite-induced immune response was associated with susceptibility rather than resistance to infection. When T cell-deficient nude mice and their normal littermates were infected with the different isolates of P. yoelii, the nude mice had lower levels of parasitemia and higher RBC counts during the early stages of these infections, and lived longer than did normal littermates after infection with the lethal isolate. These data and the data from studies of B6 and DBA/2 mice support the idea that a strong immune response may be associated with susceptibility rather than resistance to P. yoelii, at least during the early stages of the infection. The finding that a single strain of mouse may present as resistant to infection with one P. yoelii isolate yet be exquisitely susceptible to infection with another suggests that the outcome of these murine malaria infections is dependent on a dynamic interplay between host and parasite genes. Thus, when genetic variability exists in both the host and the parasite populations, as would occur in nature, there may be little directed evolutionary change toward one phenotype or another.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2025

First chromosome-level genome assembly of the colonial chordate model Botryllus schlosseri (Tunicata).

BACKGROUND: Botryllus schlosseri (Tunicata) is a colonial, laboratory model tunicate recognized for its remarkable developmental diversity, its regenerative abilities, and its peculiar genetically determined allorecognition system governed by a polymorphic locus controlling chimerism and cell parasitism. RESULTS: We report the first chromosome-level genome assembly of B. schlosseri subclade A1. By integrating long and short reads with Hi-C scaffolding, we produced both a phased diploid genome assembly and a conventional collapsed consensus sequence of 533 Mb. Of this total length, 96% belonged to 16 chromosome-scale scaffolds, with a BUSCO completeness score of 91.4%. We then compared our assembly with other high-quality tunicate genomes, revealing some synteny conservation but also extensive genomic rearrangements and a general loss of colinearity. CONCLUSIONS: The chromosome-level resolution of this assembly enhances our understanding of genome organization in colonial modular organisms. Comparative analyses highlight the dynamic nature of tunicate genomes, with conserved macrosynteny yet extensive microsyntenic rearrangements and scrambling, underscoring their rapid evolutionary trajectory. This high-quality genome assembly provides a valuable resource for exploring the unique biological features of colonial chordates, including their exceptional regenerative abilities and complex allorecognition system.

Animals↗