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PubMed2025

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↗
PubMed2026

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↗
PubMedDate not supplied

The activity of chloroquine against plasmodium falciparum in Bandar Abbas, Southern Iran, 1976.

Study to monitor the susceptibility of P. falciparum to chloroquine in south Iran was conducted in Bandar Abbas. Forty-five falciparum malaria subjects who had received 25mg. chloroquine base per kg. body weight over 3 days were followed up for 4 weeks, while three other patients for a period of 1-3 weeks. No recrudescence could be confirmed among the subjects during the follow up of the study. The mean time of asexual parasites clearance was 2.15 days. The action of chloroquine against the asexual form of P. falciparum in the present study was suspected to be slower as compared with those observed in the previous studies. However, both in vivo and limited study using the in vitro technique showed that the response of P. falciparum asexual parasites to chloroquine was still satisfactory. The study supports previous findings in Ethiopia that acquired immunity malaria had no significant effect on the asexual parasite clearance time.

Adolescent↗
PubMed1977

Life cycles of two isopora species in the canary, Serinus canarius Linnaeus.

The endogenous stages of Isospora serini Arogão and Isospora canaria Box are described from experimentally infected canaries, Serinus canarius Linnaeus. Unlike other Coccidia, the first part of the I. serini life cycle takes place in mononuclear phagocytes. Five asexual generations are described from this cell type; 2 additional asexual generations and the sexual stages take place in the intestinal epithelium. Isospora canaria, on the other hand, has a conventional coccidian life cycle in that all of the endogenous stages are in the epithelium of the small intestine, with 3 asexual generations and the sexual generation described in the duodenal epithelium. The 2 species differ in their position relative to the nucleus of the intestinal epithelial cell. Isospora serini is usually on the lumenal side of the nucleus while I. canaria is below the nucleus, toward the basement membrane. The prepatent period is 4-5 days for I. canaria and 9-10 days for I. serini. Patency lasts for 11-13 days in I. canaria infections, but duration of oocyst output is more chronic in I. serini infections, persisting for as long as 231 days. Both species have a diurnal periodicity of oocyst discharge which occurs in late afternoon and evening.

Animals↗
PubMed1978

[Life cycle of Frenkelia. IV. Pathomorphological findings in the organs of experimentally infected bank voles].

In 1975 the buzzard (Buteo buteo) was found to be the final host of Frenkelia clethrionomyobuteonis. After this discovery it became possible to investigate systematically the pathomorphology of the infection in the intermediate host, the bank vole (Clethrionomys glareolus). Fifty bank voles were infected orally with a suspension of sporocysts recovered from the faeces of experimentally infected buzzards. Each rodent receive 7000 sporocysts. Six controls each were given a faecal suspension from a non-infected buzzard. The voles were killed between 1 and 140 days after infection and examined histologically. Between the 5th and 8th day of the infection during the schizogonic multiplication of the parasite a focal necrosis of liver cells and of the liver parenchyma is observed followed by a reversible resorptive inflammation associated with siderophagia and the occurrence of giant cells. The spleen was spodogenously enlarged up to twice its normal size. There also was haemosiderosis of the bone marrow, the liver and the spleen up to 25 days after infection. At the same time the erythropoiesis in the bone morrow, the spleen and in the lymph nodes increased; there also was a lymphoid hyperplasia in spleen and lymph nodes. About 10 days after infection a reversible infiltration with lymphocytes and plasma cells developed in the liver, heart and brain. This infiltration was again detectable as perivascular and meningeal reactions in the brain after the 49th day after infection. The second asexual multiplication of the parasite was seen histologically in the grey and white matter of the central nervous system after the 18th day of infection. The developing cysts increased in size continuously thereby compressing the surrounding nervous tissue. Disseminated focal necrosis with resorptive inflammatory components was prominent in the parenchyma of the brain after the 49th day of infection. It was possible to differentiate between damage in single organs and systemic pathological lesions. The lesions in single organs were directly connected with the development of parasitic stages in the liver (schizonts) and in the brain (cysts). The generalized lesions occurred in the haemopoietic system after an impairment of the blood during the first asexual multiplication. They also occurred in the immunocytic systems after the first and during the second asexual multiplication and during the relatively late cystic phase of the parasite in the brain. The pathogenesis of the disintegration of blood cells is not clear. The immunocytic reaction can be considered an immunological response of the host against the parasite. The effect of the development of the cysts on the function and structure of the central nervous system is expected to lead to an increasing impairment of the motility of the intermediate host.

Animals↗
PubMed1977

Plasmodium falciparum gametocytes: The effect of chloroquine on their development.

Asexual erythrocytic parasites of Plasmodium falciparum are killed by chloroquine, whilst mature gametocytes are not. The gametocytes of P. falciparum take 10 days to develop to maturity and their sensitivity to chloroquine during this time was studied in vitro to investigate when the switch from susceptibility to insusceptibility occurred and to compare the responses of asexual and immature sexual parasites to the drug. 45 to 50% of asexual parasites and immature gametocytes less than one day old survived in 0.1n. mols of chloroquine per ml but 0.3n. mols of drug per ml was lethal to both. Chloroquine at 1.0n mols per ml was lethal to developing gametocytes during their first six days of growth probably due, at least in part, to the drug disorganizing the parasite's digestion of host erythrocyte haemoglobin. The drug clumped the pigment of developing gametocytes. Only immature gametocytes in the final stage of development (stage 4) survive in high chloroquine concentrations.

Animals↗
PubMed1979

The site of action of the anticoccidial salinomycin (Coxistac).

The anticoccidial salinomycin has a cidal effect against chicken coccidia. Restricted and unrestricted medication studies and histopathological examinations of chicks infected with Eimeria acervulina, E. maxima, or E. tenella showed that parasites were destroyed within host cells during asexual development. Most sporozoites failed to become trophozoites and were destroyed 30--72 hr after ingestion of oocysts. The drug also affected schizonts during initial nuclear replication by either destroying or significantly delaying their maturation. Parasites affected by the drug were distorted grossly. Drug action against gametogony was not observed histologically, but when medication was restricted to this period of the life cycle, subsequent oocyst shedding of all 3 species was reduced by 20--70% compared to unmedicated controls. When drug was provided during the entire parasite life cycle, activity against asexual stages was so complete that only a limited number of parasites survived to form gamonts, and oocyst shedding was reduced by 80--90% relative to controls. As with other ionophores, salinomycin had no effect upon rate of oocyst sporulation.

Animals↗
PubMed1977

Genetics and function of isocitrate lyase in Coprinus.

Thirteen chromosomal loci have been identified which affect acetate metabolism in Coprinus. Mutants at only two loci, acu-l and acu-7, are deficient in isocitrate lyase (ICL) (EC 4.1.3.1) activity. acu-1 mutants are unable to induce ICL because they lack acetyl-CoA synthetase which is required to convert acetate to the metabolic inducer of ICL. acu-7 is the structural gene for ICL. This was shown by selecting temperature sensitive acu+ revertants resulting from a second mutation within the acu-7 gene. One such revertant was shown to produce an ICL protein which was more thermolabile than the wild type enzyme. Other workers have postulated that ICL activity is important during asexual morphogenesis in fungi. No evidence was found for this in Coprinus. The morphological mutant oidial, which produces abundant asexual spores even in submerged culture, had the same low uninduced level of ICL activity as the wild type. Moreover, an acu-7 mutation had no effect on the expression of the oidial phenotype.

Acetates↗
PubMed2025

Nonhypermutator Cancers Access Driver Mutations Through Reversals in Germline Mutational Bias.

Cancer is an evolutionary disease driven by mutations in asexually reproducing somatic cells. In asexual microbes, bias reversals in the mutation spectrum can speed adaptation by increasing access to previously undersampled beneficial mutations. By analyzing tumors from 20 tissues, along with normal tissue and the germline, we demonstrate this effect in cancer. Nonhypermutated tumors reverse the germline mutation bias and have consistent spectra across tissues. These spectra changes carry the signature of hypoxia, and they facilitate positive selection in cancer genes. Hypermutated and nonhypermutated tumors thus acquire driver mutations differently: hypermutated tumors by higher mutation rates and nonhypermutated tumors by changing the mutation spectrum to reverse the germline mutation bias.

Neoplasms↗
PubMed2024

Non-hypermutator cancers access driver mutations through reversals in germline mutational bias.

Cancer is an evolutionary disease driven by mutations in asexually-reproducing somatic cells. In asexual microbes, bias reversals in the mutation spectrum can speed adaptation by increasing access to previously undersampled beneficial mutations. By analyzing tumors from 20 tissues, along with normal tissue and the germline, we demonstrate this effect in cancer. Non-hypermutated tumors reverse the germline mutation bias and have consistent spectra across tissues. These spectra changes carry the signature of hypoxia, and they facilitate positive selection in cancer genes. Hypermutated and non-hypermutated tumors thus acquire driver mutations differently: hypermutated tumors by higher mutation rates and non-hypermutated tumors by changing the mutation spectrum to reverse the germline mutation bias.

Journal Article↗
PubMed1979

Life cycle of Isospora rivolta (Grassi, 1879) in cats and mice.

The endogenous development of Isospora rivolta (Grassi) was studied in cats fed oocysts, and was compared with the endogenous cycle after feeding them mice infected with I. rivolta. For the mouse-induced cycle, 14 newborn cats were killed 12 to 240 h after having been fed mesenteric lymph nodes and spleens ofmice. Asexual and sexual development occurred throughout the small intestine, in epithelial cells of the villi and glands of Lieberkühn. The number of asexual generations was not determined with certainty, but there were at least 3 structurally different meronts. Type I meronts appeared at 12-48 h postinoculation (HPT). They were 8.5(6-13) x 5.1(3-6) micrometer, contained 2-8 merozoites, and divide by binary division or endodyogeny. Type II meronts were multinucleate merozoite-shaped meronts within a single parasitophorous vacuole. They were found at 48-172 HPI and measured 12.6(9-18) x 9.8(9-13) micrometer. Individual multinucleate merozoite-shaped meronts were 7-13 x 3-5 micrometer in sections and contained 2-30 slender (5.5 x 1.0 micrometer) merozoites. Type III meronts occurred at 72-192 HPI and gamonts at 72-96 HPI. Mature microgamonts measured 11.3(9-15) x 8.0(6-9) micrometer in sections and up to 21.5 x 14 micrometer in smears, and contained up to 70 microgametes. Macrogamonts measured 13.3(11-18) x 9.0(5-13) micrometer in sections and 18 x 16 micrometer in smears, and contained up to 70 microgametes. Macrogamonts measured 13.3(11-18) x 9.0(5-13) micrometer. Sporulation was completed within 24 h at 22-26 C. For the study of the oocyst-induced cycle in cats, 18 newborn cats were killed between 6 and 192 HPI. The endogenous development was essentially similar to the mouse-induced cycle, but merogony and gametogony occurred 12-48 h later than in the latter cycle. Isospora rivolta was pathogenic for newborn but not for weaned cats. Newborn cats fed 10(6) sporocysts or infected mice usually developed diarrhea 3-4 days after inoculation. Microscopically, desquamation of the tips of the villi and cryptitis were seen in the ilium and cecum in association with meronts and gamonts. For the study of the development of I. rivolta in mice, mice were killed from day 1 to 23 months after having been fed 10(5)-10(6) sporocysts, and their tissues were examined for the parasites microscopically, and by feeding to cats. The following conclusions were drawn. (A) Isospora rivolta most freqeuntly invaded the mesenteric lymph nodes ofmice and remained there for 23 months at least. Ii also invaded the spleen, liver, and skeletal muscles of mice. This species could not be passed from mouse to mouse. Sporozoites increased in size from approximately 6.8 x 4.9 micrometer on day 1 to approximately 13.4 x 6.9 micrometer on day 31 postinoculation. Division was not seen. Prepatent period was 4-7 days and patent periods ranged from 2 to several weeks.

Animals↗
PubMed1979

A malarial parasite of Australian skinks, Plasmodium mackerrasae sp. n.

Plasmodium mackerrasae sp. n. parasitizes the Australian lizards Egernia cunninghami and E. striolata (Sauria: Scincidae). Described from an experimental host, E. whitei, it produces mature schizonts containing 6--12 nuclei arranged peripherally as a rosette, and round to oval gametocytes which are equal to or slightly smaller than host cell nuclei. Both schizonts and gametocytes parasitize all cells in the erythrocyte series. Presence of pigment in both asexual and sexual stages is correlated with maturity of the host cell. Asexual forms contain a single large vacuole, whereas mature gametocytes may show 1--4 vacuoles. Plasmodium mackerrasae resembles most closely P. sasai of Japan and P. tropiduri of tropical America. It differs from P. sasai by lacking fan-shaped schizonts and by having less heavily pigmented gametocytes, and from P. tropiduri by less variability in shape and greater vacuolation of the gametocytes. Host and geographic differences further support its distinction.

Animals↗
PubMed1978

Life cycle of Mesocestoides corti in the dog (Canis familiaris).

Ten Beagle pups were each inoculated per os with 2,000 tetrathyridia of Mesocestoides corti from mice. The dogs were necropsied at 5-day intervals and the small intestine of each dog was divided into 3 equidistant sections. Adult cestodes were counted and characterized morphologically. The M corti reproduced asexually in the Beagles by longitudinal splitting of the parent scolex, separation of a new individual, and subsequent regrowth of 2 additional suckers on both the parent and newly formed scolices. Five days after the tetrathyridia were given, evidence of parent scolex division was present. The ability of M corti to reproduce asexually in the definitive host enabled rapid proliferation of new organisms, with approximately 53,000 present 45 days after inoculation.

Animals↗