RESUMO
Environmental enrichment is used to provide well-being to the animals, such as fish, in captive conditions, mimicking their natural habitat. It may influence fish behavior, physiology, and survival. In terms of reproduction, however, the relationship between environment enrichment and successful reproduction in captivity is still poorly explored in fish species. Aiming to understand any possible benefits of structural enrichment on fish reproduction, 10-days-hatched larvae of the twospot astyanax Astyanax bimaculatus were raised for 18 weeks in tanks with different elements of structural environmental enrichment (PVC pipes, stones, and artificial plants). In the 5th month of life, those animals were hormonally induced to reproduce to assess gamete formation and offspring quality. Animals raised in a sterile-reared environment (non-enriched) showed earlier spawning than the enriched one, presenting significant quantities of Postovulatory follicle complexes (POCs) and cells in atresia in female ovaries, indicating possible reproductive dysfunction or stress, as well as a greater quantity of empty testicular lumen in males, indicating great release of sperm. On the contrary, animals cultivated in enriched environments showed gonads filled with semen in males and vitellogenic oocytes in females. Furthermore, offspring from the sterile-reared group presented significant rates of larval abnormality compared to the enriched group. In conclusion, the results of this study show that environmental enrichment can interfere with the reproduction of fish in captivity, mainly by preventing early maturation of gametes, which can result in low-quality offspring and, consequently, low production of fish species.
Assuntos
Characidae , Gametogênese , Reprodução , Animais , Feminino , Masculino , Gametogênese/fisiologia , Reprodução/fisiologia , Characidae/fisiologia , Meio Ambiente , AquiculturaRESUMO
Histones are the building units of nucleosomes, which constitute chromatin. Histone post-translational modifications (PTMs) play an essential role in epigenetic gene regulation. The Plasmodium falciparum genome encodes canonical and variant histones and a collection of conserved enzymes for histone PTMs and chromatin remodeling. Herein, we profiled the P. falciparum histone PTMs during the development of gametocytes, the obligatory stage for parasite transmission. Mass spectrometric analysis of histones extracted from the early, middle, and late stages of gametocytes identified 457 unique histone peptides with 90 PTMs, of which 50% were novel. The gametocyte histone PTMs display distinct patterns from asexual stages, with many new methylation sites in histones H3 and H3.3 (e.g., K14, K18, and K37). Quantitative analyses revealed a high abundance of acetylation in H3 and H4, mono-methylation of H3/H3.3 K37, and ubiquitination of H3BK112, suggesting that these PTMs play critical roles in gametocytes. Gametocyte histones also showed extensive and unique combinations of PTMs. These data indicate that the parasite harbors distinct transcription regulation mechanisms during gametocyte development and lay the foundation for further characterization of epigenetic regulation in the life cycle of the malaria parasite.
Assuntos
Gametogênese , Histonas , Plasmodium falciparum , Processamento de Proteína Pós-Traducional , Acetilação , Epigênese Genética/genética , Gametogênese/genética , Gametogênese/fisiologia , Histonas/genética , Histonas/metabolismo , Humanos , Estágios do Ciclo de Vida/genética , Estágios do Ciclo de Vida/fisiologia , Malária Falciparum/parasitologia , Plasmodium falciparum/genética , Plasmodium falciparum/metabolismo , Plasmodium falciparum/fisiologia , Processamento de Proteína Pós-Traducional/genética , Processamento de Proteína Pós-Traducional/fisiologiaRESUMO
Gametes are cells that have the unique ability to give rise to new individuals as well as transmit (epi)genetic information across generations. Generation of functionally competent gametes, oocytes and sperm cells, depends to some extent on several fundamental processes that occur during fetal development. Direct studies on human fetal germ cells remain hindered by ethical considerations and inaccessibility to human fetal material. Therefore, the majority of our current knowledge of germ cell development still comes from an invaluable body of research performed using different mammalian species. During the last decade, our understanding of human fetal germ cells has increased due to the successful use of human pluripotent stem cells to model aspects of human early gametogenesis and advancements on single-cell omics. Together, this has contributed to determine the cell types and associated molecular signatures in the developing human gonads. In this review, we will put in perspective the knowledge obtained from several mammalian models (mouse, monkey, pig). Moreover, we will discuss the main events during human fetal (female) early gametogenesis and how the dysregulation of this highly complex and lengthy process can link to infertility later in life.
Assuntos
Infertilidade , Sêmen , Animais , Diferenciação Celular , Feminino , Gametogênese/fisiologia , Células Germinativas , Humanos , Masculino , Mamíferos , Camundongos , SuínosRESUMO
The in vitro generation of germ cells from pluripotent stem cells (PSCs) can have a substantial effect on future reproductive medicine and animal breeding. A decade ago, in vitro gametogenesis was established in the mouse. However, induction of primordial germ cell-like cells (PGCLCs) to produce gametes has not been achieved in any other species. Here, we demonstrate the induction of functional PGCLCs from rat PSCs. We show that epiblast-like cells in floating aggregates form rat PGCLCs. The gonadal somatic cells support maturation and epigenetic reprogramming of the PGCLCs. When rat PGCLCs are transplanted into the seminiferous tubules of germline-less rats, functional spermatids-that is, those capable of siring viable offspring-are generated. Insights from our rat model will elucidate conserved and divergent mechanisms essential for the broad applicability of in vitro gametogenesis.
Assuntos
Diferenciação Celular , Gametogênese , Células-Tronco Pluripotentes , Animais , Diferenciação Celular/fisiologia , Epigenômica , Gametogênese/fisiologia , Células Germinativas , Camadas Germinativas , Masculino , RatosRESUMO
Mitochondrial adrenodoxins (ADXs) are small iron-sulfur proteins with electron transfer properties. In animals, ADXs transfer electrons between an adrenodoxin reductase (ADXR) and mitochondrial P450s, which is crucial for steroidogenesis. Here we show that a plant mitochondrial steroidogenic pathway, dependent on an ADXR-ADX-P450 shuttle, is essential for female gametogenesis and early embryogenesis through a maternal effect. The steroid profile of maternal and gametophytic tissues of wild-type (WT) and adxr ovules revealed that homocastasterone is the main steroid present in WT gametophytes and that its levels are reduced in the mutant ovules. The application of exogenous homocastasterone partially rescued adxr and P450 mutant phenotypes, indicating that gametophytic homocastasterone biosynthesis is affected in the mutants and that a deficiency of this hormone causes the phenotypic alterations observed. These findings also suggest not only a remarkable similarity between steroid biosynthetic pathways in plants and animals but also a common function during sexual reproduction.
Assuntos
Adrenodoxina/metabolismo , Arabidopsis/embriologia , Ferredoxina-NADP Redutase/metabolismo , Sequência de Aminoácidos , Arabidopsis/genética , Sistema Enzimático do Citocromo P-450/metabolismo , Sistema Enzimático do Citocromo P-450/fisiologia , Transporte de Elétrons , Complexo de Proteínas da Cadeia de Transporte de Elétrons/metabolismo , Complexo de Proteínas da Cadeia de Transporte de Elétrons/fisiologia , Desenvolvimento Embrionário/genética , Gametogênese/fisiologia , Células Germinativas Vegetais/metabolismo , Mitocôndrias/metabolismo , Membranas Mitocondriais/metabolismo , Fitosteróis/biossíntese , Ligação ProteicaRESUMO
Transmission of malaria-causing parasites to mosquitoes relies on the production of gametocyte stages and their development into gametes. These stages display various microtubule cytoskeletons and the architecture of the corresponding microtubule organisation centres (MTOC) remains elusive. Combining ultrastructure expansion microscopy (U-ExM) with bulk proteome labelling, we first reconstructed in 3D the subpellicular microtubule network which confers cell rigidity to Plasmodium falciparum gametocytes. Upon activation, as the microgametocyte undergoes three rounds of endomitosis, it also assembles axonemes to form eight flagellated microgametes. U-ExM combined with Pan-ExM further revealed the molecular architecture of the bipartite MTOC coordinating mitosis with axoneme formation. This MTOC spans the nuclear membrane linking cytoplasmic basal bodies to intranuclear bodies by proteinaceous filaments. In P. berghei, the eight basal bodies are concomitantly de novo assembled in a SAS6- and SAS4-dependent manner from a deuterosome-like structure, where centrin, γ-tubulin, SAS4 and SAS6 form distinct subdomains. Basal bodies display a fusion of the proximal and central cores where centrin and SAS6 are surrounded by a SAS4-toroid in the lumen of the microtubule wall. Sequential nucleation of axonemes and mitotic spindles is associated with a dynamic movement of γ-tubulin from the basal bodies to the intranuclear bodies. This dynamic architecture relies on two non-canonical regulators, the calcium-dependent protein kinase 4 and the serine/arginine-protein kinase 1. Altogether, these results provide insights into the molecular organisation of a bipartite MTOC that may reflect a functional transition of a basal body to coordinate axoneme assembly with mitosis.
Assuntos
Axonema/ultraestrutura , Gametogênese/fisiologia , Microscopia/métodos , Centro Organizador dos Microtúbulos/ultraestrutura , Mitose/fisiologia , Plasmodium/fisiologia , Animais , Camundongos , Plasmodium/ultraestruturaRESUMO
The continued existence of Plasmodium parasites in physiologically distinct environments during their transmission in mosquitoes and vertebrate hosts requires effector proteins encoded by parasite genes to provide adaptability. Parasites utilize their robust stress response system involving heat shock proteins for their survival. Molecular chaperones are involved in maintaining protein homeostasis within a cell during stress, protein biogenesis and the formation of protein complexes. Due to their critical role in parasite virulence, they are considered targets for therapeutic interventions. Our results identified a putative P. berghei heat shock protein (HSP) belonging to the HSP40 family (HspJ62), which is abundantly induced upon heat stress and expressed during all parasite stages. To determine the role HspJ62, a gene-disrupted P. berghei transgenic line was developed (ΔHspJ62), which resulted in disruption of gametocyte formation. Such parasites were unable to form subsequent sexual stages because of disrupted gametogenesis, indicating the essential role of HspJ62 in gametocyte formation. Transcriptomic analysis of the transgenic line showed downregulation of a number of genes, most of which were specific to male or female gametocytes. The transcription factor ApiAP2 was also downregulated in ΔHspJ62 parasites. Our findings suggest that the downregulation of ApiAP2 likely disrupts the transcriptional regulation of sexual stage genes, leading to impaired gametogenesis. This finding also highlights the critical role that HspJ62 indirectly plays in the development of P. berghei sexual stages and in facilitating the conversion from the asexual blood stage to the sexual stage. This study characterizes the HspJ62 protein as a fertility factor because parasites lacking it are unable to transmit to mosquitoes. This study adds an important contribution to ongoing research aimed at understanding gametocyte differentiation and formation in parasites. The molecule adds to the list of potential drug targets that can be targeted to inhibit parasite sexual development and consequently parasite transmission.
Assuntos
Gametogênese/fisiologia , Proteínas de Choque Térmico/fisiologia , Plasmodium berghei/fisiologia , Proteínas de Protozoários/fisiologia , Animais , Feminino , Proteínas de Choque Térmico/genética , Temperatura Alta , Estágios do Ciclo de Vida , MasculinoRESUMO
Gametocytes of the malaria parasite Plasmodium are taken up by the mosquito vector with an infectious blood meal, representing a critical stage for parasite transmission. Calcium-independent protein kinases (CDPKs) play key roles in calcium-mediated signaling across the complex life cycle of the parasite. We sought to understand their role in human parasite transmission from the host to the mosquito vector and thus investigated the role of the human-infective parasite Plasmodium falciparum CDPK4 in the parasite life cycle. P. falciparum cdpk4- parasites created by targeted gene deletion showed no effect in blood stage development or gametocyte development. However, cdpk4- parasites showed a severe defect in male gametogenesis and the emergence of flagellated male gametes. To understand the molecular underpinnings of this defect, we performed mass spectrometry-based phosphoproteomic analyses of wild-type and Plasmodium falciparum cdpk4- late gametocyte stages to identify key CDPK4-mediated phosphorylation events that may be important for the regulation of male gametogenesis. We further employed in vitro assays to identify these putative substrates of Plasmodium falciparum CDPK4. This indicated that CDPK4 regulates male gametogenesis by directly or indirectly controlling key essential events, such as DNA replication, mRNA translation, and cell motility. Taken together, our work demonstrates that PfCDPK4 is a central kinase that regulates exflagellation and thereby is critical for parasite transmission to the mosquito vector. IMPORTANCE Transmission of the malaria parasite to the mosquito vector is critical for the completion of the sexual stage of the parasite life cycle and is dependent on the release of male gametes from the gametocyte body inside the mosquito midgut. In the present study, we demonstrate that PfCDPK4 is critical for male gametogenesis and is involved in phosphorylation of proteins essential for male gamete emergence. Targeting PfCDPK4 and its substrates may provide insights into achieving effective malaria transmission-blocking strategies.
Assuntos
Proteínas Quinases Dependentes de Cálcio-Calmodulina/metabolismo , Gametogênese/fisiologia , Mosquitos Vetores , Plasmodium falciparum/enzimologia , Plasmodium falciparum/metabolismo , Animais , Sinalização do Cálcio , Proteínas Quinases Dependentes de Cálcio-Calmodulina/genética , Culicidae , Gametogênese/genética , Células Germinativas/metabolismo , Estágios do Ciclo de Vida , Malária Falciparum/parasitologia , Malária Falciparum/transmissão , Masculino , Fosforilação , Plasmodium falciparum/genética , Proteínas de Protozoários/genéticaRESUMO
Ecosystems and their biota operate on cyclic rhythms, often entrained by predictable, small-scale changes in their natural environment. Recording and understanding these rhythms can detangle the effect of human induced shifts in the climate state from natural fluctuations. In this study, we assess long-term patterns of reproductive investment in the Antarctic sea urchin, Sterechinus neumayeri, in relation to changes in the environment to identify drivers of reproductive processes. Polar marine biota are sensitive to small changes in their environment and so serve as a barometer whose responses likely mirror effects that will be seen on a wider global scale in future climate change scenarios. Our results indicate that seasonal reproductive periodicity in the urchin is underpinned by a multiyear trend in reproductive investment beyond and in addition to, the previously reported 18-24 month gametogenic cycle. Our model provides evidence that annual reproductive investment could be regulated by an endogenous rhythm since environmental factors only accounted for a small proportion of the residual variation in gonad index. This research highlights a need for multiyear datasets and the combination of biological time series data with large-scale climate metrics that encapsulate multi-factorial climate state shifts, rather than using single explanatory variables to inform changes in biological processes.
Assuntos
Reprodução , Ouriços-do-Mar/fisiologia , Animais , Regiões Antárticas , Mudança Climática , Ecossistema , Feminino , Gametogênese/fisiologia , Masculino , Estações do AnoRESUMO
Gametogenesis is one of the most extreme cellular differentiation processes that takes place in Drosophila male and female germlines. This process begins at the germline stem cell, which undergoes asymmetric cell division (ACD) to produce a self-renewed daughter that preserves its stemness and a differentiating daughter cell that undergoes epigenetic and genomic changes to eventually produce haploid gametes. Research in molecular genetics and cellular biology are beginning to take advantage of the continually advancing genomic tools to understand: (1) how germ cells are able to maintain their identity throughout the adult reproductive lifetime, and (2) undergo differentiation in a balanced manner. In this review, we focus on the epigenetic mechanisms that address these two questions through their regulation of germline-soma communication to ensure germline stem cell identity and activity.
Assuntos
Células-Tronco Germinativas Adultas/fisiologia , Diferenciação Celular/genética , Gametogênese/genética , Células-Tronco Germinativas Adultas/metabolismo , Animais , Divisão Celular Assimétrica , Drosophila/embriologia , Proteínas de Drosophila/metabolismo , Drosophila melanogaster/metabolismo , Epigênese Genética/genética , Epigenômica/métodos , Gametogênese/fisiologia , Expressão Gênica/genética , Regulação da Expressão Gênica no Desenvolvimento/genética , Células Germinativas/metabolismo , Células-Tronco/citologiaRESUMO
Anti-Müllerian hormone (Amh) plays an important role in gonadal function. Amh deficiency causes severe gonadal dysgenesis and dysfunction in zebrafish, with gonadal hypertrophy in both sexes. However, its mechanism of action remains unknown. Intriguingly, the Amh cognate type II receptor (Amhr2) is missing in the zebrafish genome, in sharp contrast to other species. Using a series of zebrafish mutants (amh, fshb, fshr and lhcgr), we provided unequivocal evidence for actions of Amh, via modulation of gonadotropin signaling, on both germ cell proliferation and differentiation. The gonadal hypertrophy in amh mutants was abolished in the absence of Fshr in females or Fshr/Lhcgr in males. Furthermore, we demonstrated that knockout of bmpr2a, but not bmpr2b, phenocopied all phenotypes of the amh mutant in both sexes, including gonadal hypertrophy, hyperproliferation of germ cells, retarded gametogenesis and reduced fshb expression. In summary, the present study provided comprehensive genetic evidence for an intimate interaction of gonadotropin and Amh pathways in gonadal homeostasis and gametogenesis and for Bmpr2a as the possible missing link for Amh signaling in zebrafish.
Assuntos
Hormônio Antimülleriano/metabolismo , Receptores de Proteínas Morfogenéticas Ósseas Tipo II/metabolismo , Gametogênese/fisiologia , Células Germinativas/metabolismo , Gonadotropinas/metabolismo , Transdução de Sinais/fisiologia , Proteínas de Peixe-Zebra/metabolismo , Peixe-Zebra/metabolismo , Animais , Hormônio Antimülleriano/genética , Receptores de Proteínas Morfogenéticas Ósseas Tipo II/genética , Feminino , Células Germinativas/citologia , Gonadotropinas/genética , Masculino , Peixe-Zebra/genética , Proteínas de Peixe-Zebra/genéticaRESUMO
RNA systems biology is marked by a myriad of cellular processes mediated by small and long non-coding RNAs. Small non-coding RNAs include siRNAs (small interfering RNAs), miRNAs (microRNAs), tRFs(tRNA derived fragments), and piRNAs (PIWI-interacting RNAs). piRNAs are vital for the maintenance of the germ-line integrity and repress the transposons either transcriptionally or post-transcriptionally. Studies based on model organisms have shown that defects in the piRNA pathway exhibit impaired gametogenesis and loss of fertility. piRNA biogenesis is marked by transcription of precursor molecules and their subsequent processing in the cytoplasm to generate mature piRNAs. Their biogenesis is unique and complex, which involves non-canonical transcription and self-amplification mechanisms such as the ping-pong cycle. piRNA biogenesis is different in somatic and germ cells and involves the role of cytoplasmic granules in addition to mitochondria. In this review, we discuss the biogenesis and maturation of piRNAs in various cytoplasmic granules such as Yb and nuage bodies. Also, we review the role of P bodies, stress granules, and P granules, and membrane-bound compartments such as mitochondria and exosomes in piRNA biogenesis.
Assuntos
Grânulos Citoplasmáticos/metabolismo , Exossomos/metabolismo , Células Germinativas/metabolismo , Mitocôndrias/metabolismo , RNA Interferente Pequeno/metabolismo , Animais , Fertilidade/fisiologia , Gametogênese/fisiologia , HumanosRESUMO
SARS-CoV-2 infection and pregnancy has been the topic of hundreds of publications over the last several months; however, few studies have focused on the implications of infection in early pregnancy and reproductive tissues. Here, we analyzed available evidence pertaining to SARS-CoV-2 infection, in early pregnancy, and in reproductive tissues. We searched PubMed and Embase databases in accordance with guidelines of Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) for publications from inception to June 4, 2020. Four reviewers screened titles and abstracts and obtained full-text articles for analysis. Sixty-two studies were included in the review. Biological plausibility for infection with SARS-CoV-2 exists in testis, ovaries, and placenta as they express ACE2 receptor activity. In males, SARS-CoV-2 infection could lead to functional abnormalities leading to spermatogenic failure and male infertility. In females, an alteration of the ACE2 cascade via SARS-CoV-2 infection could lead to impairment in important follicular and luteal processes. There is also evidence of significant placental pathology in SARS-CoV-2 infection, but it is unclear what effects there may be for early pregnancy, though available data suggest less severe effects compared to other respiratory virus outbreaks. Further investigation is needed regarding SARS-CoV-2 in reproductive function and early pregnancy.
Assuntos
Enzima de Conversão de Angiotensina 2/metabolismo , COVID-19/virologia , Gametogênese/fisiologia , Placenta/metabolismo , Complicações Infecciosas na Gravidez/virologia , SARS-CoV-2/fisiologia , Espermatozoides/metabolismo , Feminino , Humanos , Masculino , Pandemias , Placenta/patologia , Placenta/virologia , Gravidez , Reprodução , Espermatozoides/patologia , Espermatozoides/virologiaRESUMO
Anti-Müllerian hormone (AMH/Amh) plays a role in gonadal differentiation and function across vertebrates. In zebrafish we demonstrated that Amh deficiency caused severe gonadal dysgenesis and dysfunction. The mutant gonads showed extreme hypertrophy with accumulation of early germ cells in both sexes, namely spermatogonia in the testis and primary growth oocytes in the ovary. In amh mutant females, the folliculogenesis was normal in young fish but receded progressively in adults, which was accompanied by progressive decrease in follicle-stimulating hormone (fshb) expression. Interestingly the expression of fshb increased in the pituitary of juvenile amh mutant males but decreased in adults. The upregulation of fshb in mutant male juveniles was likely one of the mechanisms for triggering gonadal hypergrowth, whereas the downregulation of fshb in adults might involve a negative feedback by gonadal inhibin. Further analysis using mutants of fshb and growth differentiation factor 9 (gdf9) provided evidence for a role of FSH in triggering ovarian hypertrophy in young female amh mutant as well. In summary, the present study provided comprehensive genetic evidence for dual roles of Amh in controlling zebrafish gonadal homeostasis and gametogenesis in both sexes. Amh suppresses proliferation or accumulation of early germ cells (spermatogonia in testis and primary growth oocytes in ovary) while promoting their exit to advanced stages, and its action may involve both endocrine and paracrine pathways.
Assuntos
Hormônio Antimülleriano/fisiologia , Gametogênese/fisiologia , Homeostase/fisiologia , Proteínas de Peixe-Zebra/fisiologia , Ativinas/fisiologia , Animais , Hormônio Antimülleriano/deficiência , Hormônio Antimülleriano/genética , Sequência de Bases , Sistemas CRISPR-Cas , Retroalimentação Fisiológica , Feminino , Hormônio Foliculoestimulante/biossíntese , Hormônio Foliculoestimulante/genética , Técnicas de Inativação de Genes , Fator 9 de Diferenciação de Crescimento/genética , Hipertrofia , Infertilidade Feminina/genética , Infertilidade Masculina/genética , Inibinas/fisiologia , Masculino , Ovário/metabolismo , Ovário/patologia , Comunicação Parácrina , Adeno-Hipófise/metabolismo , Maturidade Sexual/genética , Testículo/metabolismo , Testículo/patologia , Peixe-ZebraRESUMO
Spatiotemporally regulated callose deposition is an essential, genetically programmed phenomenon that promotes pollen development and functionality. Severe male infertility is associated with deficient callose biosynthesis, highlighting the significance of intact callose deposition in male gametogenesis. The molecular mechanism that regulates the crucial role of callose in production of functional male gametophytes remains completely unexplored. Here, we provide evidence that the gradual upregulation of a previously uncharacterized cotton (Gossypium hirsutum) pollen-specific SKS-like protein (PSP231), specifically at the post pollen-mitosis stage, activates callose biosynthesis to promote pollen maturation. Aberrant PSP231 expression levels caused by either silencing or overexpression resulted in late pollen developmental abnormalities and male infertility phenotypes in a dose-dependent manner, highlighting the importance of fine-tuned PSP231 expression. Mechanistic analyses revealed that PSP231 plays a central role in triggering and fine-tuning the callose synthesis and deposition required for pollen development. Specifically, PSP231 protein sequesters the cellular pool of RNA-binding protein GhRBPL1 to destabilize GhWRKY15 mRNAs, turning off GhWRKY15-mediated transcriptional repression of GhCalS4/GhCalS8 and thus activating callose biosynthesis in pollen. This study showed that PSP231 is a key molecular switch that activates the molecular circuit controlling callose deposition toward pollen maturation and functionality and thereby safeguards agricultural crops against male infertility.
Assuntos
Gametogênese/genética , Gametogênese/fisiologia , Glucanos/biossíntese , Gossypium/fisiologia , Proteínas de Plantas/genética , Pólen/crescimento & desenvolvimento , Pólen/genética , Produtos Agrícolas/citologia , Produtos Agrícolas/genética , Produtos Agrícolas/fisiologia , Regulação da Expressão Gênica de Plantas , Genes de Plantas , Glucanos/genética , Gossypium/citologia , Gossypium/genética , Proteínas de Plantas/metabolismo , Pólen/citologia , Pólen/metabolismoRESUMO
Ambient temperature modulates reproductive processes, especially in poikilotherms such as teleosts. Consequently, global warming is expected to impact the reproductive function of fish, which has implications for wild population dynamics, fisheries and aquaculture. In this extensive review spanning tropical and cold-water environments, we examine the impact of higher-than-optimal temperatures on teleost reproductive development and physiology across reproductive stages, species, generations and sexes. In doing so, we demonstrate that warmer-than-optimal temperatures can affect every stage of reproductive development from puberty through to the act of spawning, and these responses are mediated by age at spawning and are associated with changes in physiology at multiple levels of the brain-pituitary-gonad axis. Response to temperature is often species-specific and changes with environmental history/transgenerational conditioning, and the amplitude, timing and duration of thermal exposure within a generation. Thermally driven changes to physiology, gamete development and maturation typically culminate in poor sperm and oocyte quality, and/or advancement/delay/inhibition of ovulation/spermiation and spawning. Although the field of teleost reproduction and temperature is advanced in many respects, we identify areas where research is lacking, especially for males and egg quality from "omics" perspectives. Climate-driven warming will continue to disturb teleost reproductive performance and therefore guide future research, especially in the emerging areas of transgenerational acclimation and epigenetic studies, which will help to understand and project climate change impacts on wild populations and could also have implications for aquaculture.
Assuntos
Mudança Climática , Peixes/fisiologia , Gametogênese/fisiologia , Reprodução/fisiologia , Temperatura , Aclimatação/fisiologia , Animais , Pesqueiros , Dinâmica PopulacionalRESUMO
Acentrosomal meiosis in oocytes represents a gametogenic challenge, requiring spindle bipolarization without predefined bipolar cues. While much is known about the structures that promote acentrosomal microtubule nucleation, less is known about the structures that mediate spindle bipolarization in mammalian oocytes. Here, we show that in mouse oocytes, kinetochores are required for spindle bipolarization in meiosis I. This process is promoted by oocyte-specific, microtubule-independent enrichment of the antiparallel microtubule crosslinker Prc1 at kinetochores via the Ndc80 complex. In contrast, in meiosis II, cytoplasm that contains upregulated factors including Prc1 supports kinetochore-independent pathways for spindle bipolarization. The kinetochore-dependent mode of spindle bipolarization is required for meiosis I to prevent chromosome segregation errors. Human oocytes, where spindle bipolarization is reportedly error prone, exhibit no detectable kinetochore enrichment of Prc1. This study reveals an oocyte-specific function of kinetochores in acentrosomal spindle bipolarization in mice, and provides insights into the error-prone nature of human oocytes.
Assuntos
Cinetocoros/metabolismo , Proteínas Associadas aos Microtúbulos/metabolismo , Oócitos/metabolismo , Fuso Acromático/metabolismo , Animais , Proteínas de Ciclo Celular/metabolismo , Segregação de Cromossomos , Proteínas do Citoesqueleto/metabolismo , Feminino , Gametogênese/fisiologia , Meiose/fisiologia , Camundongos , Microtúbulos/metabolismo , Proteínas Nucleares/metabolismoRESUMO
Clonal animals do not sequester a germ line during embryogenesis. Instead, they have adult stem cells that contribute to somatic tissues or gametes. How germ fate is induced in these animals, and whether this process is related to bilaterian embryonic germline induction, is unknown. We show that transcription factor AP2 (Tfap2), a regulator of mammalian germ lines, acts to commit adult stem cells, known as i-cells, to the germ cell fate in the clonal cnidarian Hydractinia symbiolongicarpus Tfap2 mutants lacked germ cells and gonads. Transplanted wild-type cells rescued gonad development but not germ cell induction in Tfap2 mutants. Forced expression of Tfap2 in i-cells converted them to germ cells. Therefore, Tfap2 is a regulator of germ cell commitment across germ line-sequestering and germ line-nonsequestering animals.
Assuntos
Células-Tronco Adultas/citologia , Gametogênese/fisiologia , Células Germinativas/citologia , Gônadas/embriologia , Hidrozoários/embriologia , Fator de Transcrição AP-2/fisiologia , Células-Tronco Adultas/metabolismo , Animais , Feminino , Gametogênese/genética , Regulação da Expressão Gênica no Desenvolvimento , Gônadas/citologia , Hidrozoários/citologia , Hidrozoários/genética , Masculino , Fator de Transcrição AP-2/genéticaRESUMO
BACKGROUND: The intraerythrocytic development cycle (IDC) of the rodent malaria Plasmodium chabaudi is coordinated with host circadian rhythms. When this coordination is disrupted, parasites suffer a 50% reduction in both asexual stages and sexual stage gametocytes over the acute phase of infection. Reduced gametocyte density may not simply follow from a loss of asexuals because investment into gametocytes ("conversion rate") is a plastic trait; furthermore, the densities of both asexuals and gametocytes are highly dynamic during infection. Hence, the reasons for the reduction of gametocytes in infections that are out-of-synch with host circadian rhythms remain unclear. Here, two explanations are tested: first, whether out-of-synch parasites reduce their conversion rate to prioritize asexual replication via reproductive restraint; second, whether out-of-synch gametocytes experience elevated clearance by the host's circadian immune responses. METHODS: First, conversion rate data were analysed from a previous experiment comparing infections of P. chabaudi that were in-synch or 12 h out-of-synch with host circadian rhythms. Second, three new experiments examined whether the inflammatory cytokine TNF varies in its gametocytocidal efficacy according to host time-of-day and gametocyte age. RESULTS: There was no evidence that parasites reduce conversion or that their gametocytes become more vulnerable to TNF when out-of-synch with host circadian rhythms. CONCLUSIONS: The factors causing the reduction of gametocytes in out-of-synch infections remain mysterious. Candidates for future investigation include alternative rhythmic factors involved in innate immune responses and the rhythmicity in essential resources required for gametocyte development. Explaining why it matters for gametocytes to be synchronized to host circadian rhythms might suggest novel approaches to blocking transmission.
Assuntos
Ritmo Circadiano , Eritrócitos/parasitologia , Malária/parasitologia , Plasmodium chabaudi/fisiologia , Fator de Necrose Tumoral alfa/administração & dosagem , Animais , Ritmo Circadiano/imunologia , Feminino , Citometria de Fluxo , Gametogênese/fisiologia , Modelos Lineares , Malária/sangue , Malária/imunologia , Masculino , Merozoítos/fisiologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Mutantes , Plasmodium chabaudi/genética , Plasmodium chabaudi/crescimento & desenvolvimento , Plasmodium chabaudi/imunologia , Distribuição Aleatória , Reação em Cadeia da Polimerase em Tempo Real , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Fatores de Tempo , Fator de Necrose Tumoral alfa/sangue , Fator de Necrose Tumoral alfa/imunologiaRESUMO
The genetic codes inscribed during two key developmental processes, namely gametogenesis and embryogenesis, are believed to determine subsequent development and survival of adult life. Once the embryo is formed, its further development mainly depends on its intrinsic characteristics, maternal environment (the endometrial receptivity), and the embryo-maternal interactions established during each phase of development. These developmental processes are under strict genetic regulation that could be manifested temporally and spatially depending on the physiological and developmental status of the cell. MicroRNAs (miRNAs), one of the small non-coding classes of RNAs, approximately 19-22 nucleotides in length, are one of the candidates for post-transcriptional developmental regulators. These tiny non-coding RNAs are expressed in ovarian tissue, granulosa cells, testis, oocytes, follicular fluid, and embryos and are implicated in diverse biological processes such as cell-to-cell communication. Moreover, accumulated evidences have also highlighted that miRNAs can be released into the extracellular environment through different mechanisms facilitating intercellular communication. Therefore, understanding miRNAs mediated regulatory mechanisms during gametogenesis and embryogenesis provides further insights about the molecular mechanisms underlying oocyte/sperm formation, early embryo development, and implantation. Thus, this review highlights the role of miRNAs in mammalian gametogenesis and embryogenesis and summarizes recent findings about miRNA-mediated post-transcriptional regulatory mechanisms occurring during early mammalian development.