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Genomic and evolutionary basis of parthenogenesis in a disease-vector tick species.

Haemaphysalis longicornis is an important tick species and pathogen vector characterized by the co-circulation of triploid parthenogenetic and diploid bisexual strains. However, the evolutionary basis of parthenogenesis in this species is unclear. Here we report reference-quality, haplotype-resolved genome assemblies of the parthenogenetic strain and two reference-quality genomes of the bisexual strains. Comparative genomic analysis revealed high collinearity between the parthenogenetic and bisexual genomes, with a stable chromosomal architecture maintained among the three haplotypes of the parthenogenetic strain. The parthenogenetic H. longicornis genome exhibited a major expansion in cell cycle-related gene families, including the inhibitor of apoptosis protein (IAP) family, but was characterized by a contraction in other gene families. Population resequencing of 179 individuals revealed two distinct subpopulations, with chromosome 7 harbouring high genetic differentiation and several candidate genes probably associated with parthenogenesis. Functional experiments showed that knockdown of the BIRC5 gene, a member of the IAP family, suppressed oviposition in both strains, with the parthenogenetic strain exhibiting milder adverse effects probably due to a stronger transcriptional response. Overall, our results reveal the genomic and evolutionary features associated with polyploid parthenogenesis in H. longicornis.

Animals

Parthenogenesis.

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Amphibians

[Research on the artificial regulation of sex in animals in the USSR].

The problem of artificial sex control was cardinally solved only for the silkworm among the domestic animals. The artificial sex control is realized by means of several methods. The artificial ameiotic parthenogenesis allows to obtain isogenic parthenogenetic progeny of only female sex. The meiotic parthenogenesis, on the contrary, gives only male progeny characterized by homozygosis by all genes. As a result of androgenesis with the participation of ooplasm and male nuclear material, only male progeny develops as well. Sex marked strains in which the female and male eggs are coloured in different may were obtained by means of translocation of the dominant genes controlling the egg colour on W chromosome determining the female sex. This allows readily to pick out the eggs of desirable sex only with the help of photoelectric equipment. The males of a specially raised strain balanced by two non-allelic sex-linked lethals, when being crossed with the females of any other strain, give male progeny only. The developed methods of sex control have found wide application in theoretical investigations of various directions and practical sericulture.

Animals

The twofold cost of sex reconsidered: meiotic mechanisms protect anisogamous populations from invasion by thelytoky.

Most multicellular animals practice anisogamy (fertilization between eggs and sperm). When mothers produce sons and daughters at a 1:1 ratio, the "twofold cost of males" arises because males do not directly contribute to population growth. If thelytokous parthenogens producing only daughters invade a population, they should spread rapidly. Although thelytoky has repeatedly evolved across invertebrate and vertebrate taxa, it remains a minority. Why? The evolutionary transition from anisogamy to thelytoky requires eggs to initiate embryonic development without fertilization. However, in metazoan animals, meiotic metaphase (MM) arrest halts oogenesis midway and normally resumes only after stimulation by sperm penetration. Empirical and experimental evidences indicate that release of MM arrest without fertilization is extremely difficult, providing a strong mechanistic barrier against parthenogenesis. Even if MM arrest were released, oogenesis would proceed to produce either a haploid embryo or a diploid embryo through refusion with the second polar body (terminal fusion automixis). Outbred species typically accumulate more than one lethal equivalent of recessive deleterious alleles per genome as heterozygotes. Upon transition to haploid or automictic development, these recessive lethals normally masked in outbred diploids would be exposed simultaneously, causing embryonic death and creating the next barrier. Thus, thelytoky cannot be achieved simply by modification of the existing meiotic system; instead, other mechanisms, such as apomixis, that bypass meiosis are required. Mathematical models and simulations support this "meiotic constraint" hypothesis. Combined with recently proposed immediate benefits of anisogamy and traditional genetic benefits (e.g., Red Queen), it may largely explain the maintenance of costly anisogamy.

Animals

[Maturation of the female Tetrix undulata (Swrb) (Orthoptera, Tetrigidae): influence of the male and copulation:parthenogenetic egg-laying].

The percentage of laying females and laying time, are compared between mature females (diapause break by chilling) and diapause strain females (diapause not broken by chilling) reared with mature male or diapause male or without male. For the same physiological state of the females (mature or diapause) there is no difference in the percentage of females laying, when they are reared with mature male or with diapause one or none; but the laying time is shortest with mature male, longer with male in diapause, even longer without male. Parthenogenetic egg-pods can be obtain. Rearing with mature males does not break the reproductive diapause of females. In parthenogenetic egg-pods the number of eggs is short for low diapause females; greater for mature ones and greatest for females with strong diapause broken by a corpus allatum implant of mature female of Locusta migratoria. Corpus allatum of the low diapause strain of females of Tetrix undulata have less activity than that of mature females. Few parthenogenetic eggs develop, even less hatch. In Tetrix undulata parthenogenesis is accidental.

Animals

Somatic cell origin of teratocarcinomas.

Malignant teratocarcinomas arise from developmentally totipotent normal stem cells. Whether the targets are embryonal somatic cells or germinal cells has long been a matter of controversy. Past experiments on teratocarcinoma induction by ectopic grafting of early rodent embryos or fetal germinal ridges have remained ambiguous because embryos ordinarily soon form germ cells, and parthenogenetic germ cells form "embryos." In order to interrupt the developmental cycle at its most telling point, day 6 (egg-cylinder stage) mouse embryos of genetically sterile types were grafted; in such grafts, only a terminal residue of totipotent embryonal somatic ("ectoderm") cells is available, and subsequent germ cell development is severely impaired. One graft series, from S1(J)/+ matings, comprised 25% S1(J)/S1(J) presumptive sterile embryos; these grafts formed tumors containing embryonal carcinoma cells as often (47%) as did control +/+ grafts (41%) on the same genetic background. In another series, from W/+ matings, tumors of the sterile W/W genotype were individually identified by means of a closely linked marker, phosphoglucomutase (PGM, EC 2.7.5.1; Pgm-1 locus), coding for electrophoretic enzyme variants and incorporated into the stock. Four tumors were obtained (out of 16) that had the PGM-1D phenotype diagnostic for W/W, and that also contained embryonal carcinoma cells. Therefore, the malignancy arises here in susceptible somatic embryonal stem cells at the terminal stage of their capacity for totipotency. Other teratocarcinomas-whether induced or spontaneous-of ostensible germ-cell origin by parthenogenesis may also depend upon development of the same somatic target cells before neoplastic conversion can occur. A general model based on these experiments is proposed for all malignancies: Malignant transformation of a particular kind of normal stem cell may be possible only when that stem cell has progressed to the threshold of further differentiation.

Animals

The ecology, evolution, and physiology of Cardinium: a widespread heritable endosymbiont of invertebrates.

Candidatus Cardinium hertigii (Cardinium) are maternally transmitted obligate intracellular bacteria found in a wide range of invertebrate hosts, including arthropods and nematodes. Infection with Cardinium has substantial consequences for host biology, with many strains manipulating host reproduction to favor symbiont transmission by (i) feminizing male hosts, (ii) altering host sex allocation, (iii) inducing parthenogenesis, or (iv) causing cytoplasmic incompatibility. Other Cardinium strains can confer benefits to their host or alter host behavior. Cardinium-modified host phenotypes can result in selective sweeps of cytological elements through host populations and potentially reinforce host speciation. Cardinium has potential for applications in controlling arthropod pest species and arthropod-vectored disease transmission, although much remains to be explored regarding Cardinium physiology and host interactions. In this review, we provide an overview of Cardinium evolution and host distribution. We describe the various host phenotypes associated with Cardinium and how biological and environmental factors influence these symbioses. We also provide an overview of Cardinium metabolism, physiology, and potential mechanisms for interactions with hosts based on recent studies using genomics and transcriptomics. Finally, we discuss new methodologies and directions for Cardinium research, including improving our understanding of Cardinium physiology, response to environmental stress, and potential for controlling arthropod pest populations.

Symbiosis

Positive selection and relaxed purifying selection contribute to rapid evolution of sex-biased genes in green seaweed Ulva.

BACKGROUND: The evolution of differences in gamete size and number between sexes is a cornerstone of sexual selection theories. The green macroalga Ulva, with incipient anisogamy and parthenogenetic gametes, provides a unique system to investigate theoretical predictions regarding the evolutionary pressures that drive the transition from isogamy to anisogamy, particularly in relation to gamete size differentiation and sexual selection. Its minimal gamete dimorphism and facultative parthenogenesis enable a rare window into early evolutionary steps toward anisogamy. RESULTS: By analyzing the expression profiles of sex-biased genes (SBGs) during gametogenesis, we found that SBGs evolve faster than unbiased genes, driven by higher rates of non-synonymous substitution (dN), indicating that SBGs are under stronger selective pressures. Mating type minus-biased genes (mt-BGs) exhibit higher dN/dS values than mating type plus-biased genes (mt+BGs), suggesting stronger selective pressures on mt-BGs, although this difference was not statistically significant (P = 0.08). Using branch-site and RELAX models, we found positive selection and relaxed purifying selection acting on a significant proportion of SBGs, particularly those associated with flagella function. CONCLUSIONS: This study highlights the selective pressures shaping anisogamy and provides insights into the molecular mechanisms underlying its evolution. The faster evolution of SBGs, particularly mt-BGs, and the positive selection on genes associated with motility, such as those related to flagella function, suggest the importance of enhanced gamete motility in the transition to anisogamy. These findings contribute to our understanding of sexual selection and the evolutionary forces that drive the differentiation of gamete size and number between sexes.

Selection, Genetic

Mutation accumulation in a hybrid parthenogenetic vertebrate.

Asexual lineages are thought to experience elevated extinction rates compared with sexual species, yet direct evidence for the underlying genetic causes remains scarce. Muller's ratchet predicts that the absence of recombination in asexual organisms facilitates the accumulation of deleterious mutations, thereby reducing long-term fitness. Here, we test this hypothesis in the hybrid-origin, parthenogenetic whiptail lizard Aspidoscelis tesselatus by integrating short-read RNAseq and long-read IsoSeq data from both the asexual lineage and its parental sexual species. We reconstructed phased transcripts for A. tesselatus to quantify mutation accumulation relative to the parental sexual species. Comparative analyses revealed elevated ω ratios in both parental genomic complements (subgenomes) of the parthenogenetic lineage, consistent with accelerated accumulation of nonsynonymous mutations. Structural variant analyses identified multiple indels in expressed transcripts predicted to disrupt protein domains. Functional annotation indicated that genes affected by both single-nucleotide variants and indels were enriched for roles in chromatin organization, apoptosis regulation, and transcriptional control. While both parental subgenomes showed similar evolutionary patterns, the maternal complement exhibited more structural and missense mutations than the paternal complement. Together, these results provide evidence that mutations accumulate in asexual A. tesselatus in genes involved in core cellular functions, supporting theoretical predictions that Muller's ratchet contributes to mutation accumulation in asexual lineages.

Animals

The release of sexual conflict after sex loss is associated with evolutionary changes in gene expression.

Sexual conflict can arise because males and females, while sharing most of their genome, can have different phenotypic optima. Sexually dimorphic gene expression may help reduce conflict, but the expression of many genes may remain sub-optimal owing to unresolved tensions between the sexes. Asexual lineages lack such conflict, making them relevant models for understanding the extent to which sexual conflict influences gene expression. We investigate the evolution of sexual conflict subsequent to sex loss by contrasting the gene expression patterns of sexual and asexual lineages in the pea aphid Acyrthosiphon pisum. Although asexual lineages of this aphid produce a small number of males in autumn, their mating opportunities are limited because of geographic isolation between sexual and asexual lineages. Therefore, gene expression in parthenogenetic females of asexual lineages is no longer constrained by that of other morphs. We found that the expression of genes in males from asexual lineages tended towards the parthenogenetic female optimum, in agreement with theoretical predictions. Surprisingly, males and parthenogenetic females of asexual lineages overexpressed genes normally found in the ovaries and testes of sexual morphs. These changes in gene expression in asexual lineages may arise from the relaxation of selection or the dysregulation of gene networks otherwise used in sexual lineages.

Animals

Development of parthenogenetic membranes in double-yolked and injected chicken eggs.

Development of parthenogenetic eggs is expressed in a Dark Cornish stock by either membrane or embryo formation. Double-yolked eggs have membranes developing in zero, one, or two yolks. The incidence of double-yolked eggs with two membranes was higher than expected when compared with the incidence of single-yolked eggs from the same hens. Membrane formation was increased over that of the controls by injecting saline, Ringer's solution, or ground crude membranes. Yolk and membranes filtered through a 3 mu filter or autoclaved did not increase membrane formation over that of the controls. Fertile membranes behaved like parthenogenetic membranes.

Animals

The involvement of calcium in the activation of mammalian oocytes.

Mouse oocytes with cumulus cells intact were parthenogenetically activated following release from the oviduct into calcium-free medium. The proportion of activated oocytes increased with post ovulatory age both for oocytes initially exposed to calcium-free and calcium-containing medium (control). Apart from oocytes released shortly after ovulation (approximately 1 h) when less than 1% of the oocytes from treated and control were activated, activation was always higher in oocytes incubated in calcium-free medium (p less than 0.001). The omission of magnesium from the medium had no effect on the activation response of oocytes obtained approximately 3 h after ovulation but its absence did increase the activation rate of oocytes of later post ovulatory age (approximately 9 h after ovulation) although it was still lower than that obtained with media devoid of calcium. When the extracellular calcium was replaced by other divalent cations (strontium, barium and manganese) high rates of activation were obtained even at post ovulatory times which produced relatively low rates of activation in calcium-free medium alone. Similar results were obtained when hamster oocytes were exposed to all the aforementioned treatments. It is concluded that calcium plays an essential role in the activation of the mammalian oocyte but the mechanism of its action remains obscure. Further development of oocytes activated by calcium-free treatment was limited and was similar to that of oocytes activated in other ways.

Animals

Experimental activation of ascidian eggs.

The effects of the ionophore A23187 on the activation of the eggs of Ascidia malaca have been studied. No common external ion in the sea water is found to be essential for the activation but lanthanum and manganese inhibit the response. These observations support the interpretation that activation of these eggs results from changes in free intracellular calcium levels. This has led to the prediction of two other activating treatments, namely high external calcium and addition of theophylline.

Animals