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Most heritable information in eukaryotic cells is encoded in the nuclear genome, with inheritance patterns following classic Mendelian segregation. Genomes residing in the cytoplasm, however, prove to be a peculiar exception to this rule. Cytoplasmic genetic elements are generally maternally inherited, although there are several exceptions where these are paternally, biparentally or doubly-uniparentally inherited. In this review, we examine the diversity and peculiarities of cytoplasmically inherited genomes, and the broad evolutionary consequences that non-Mendelian inheritance brings. We first explore the origins of vertical transmission and uniparental inheritance, before detailing the vast diversity of cytoplasmic inheritance systems across Eukaryota. We then describe the evolution of genomic organisation across lineages, how this process has been shaped by interactions with the nuclear genome and population genetics dynamics. Finally, we discuss how both nuclear and cytoplasmic genomes have evolved to co-inhabit the same host cell via one of the longest symbiotic processes, and all the opportunities for intergenomic conflict that arise due to divergence in inheritance patterns. In sum, we cannot understand the evolution of eukaryotes without understanding hereditary symbiosis.

The hologenome concept of evolution postulates that the holobiont (host plus symbionts) with its hologenome (host genome plus microbiome) is a level of selection in evolution. Multicellular organisms can no longer be considered individuals by the classical definitions of the term. Every natural animal and plant is a holobiont consisting of the host and diverse symbiotic microbes and viruses. Microbial symbionts can be transmitted from parent to offspring by a variety of methods, including via cytoplasmic inheritance, coprophagy, direct contact during and after birth, and the environment. A large number of studies have demonstrated that these symbionts contribute to the anatomy, physiology, development, innate and adaptive immunity, and behavior and finally also to genetic variation and to the origin and evolution of species. Acquisition of microbes and microbial genes is a powerful mechanism for driving the evolution of complexity. Evolution proceeds both via cooperation and competition, working in parallel.

Modern evolutionary biology is founded on the Mendelian-genetic model of inheritance, but it is now clear that this model is incomplete. Empirical evidence shows that environment (encompassing all external influences on the genome) can impose transgenerational effects and generate heritable variation for a broad array of traits in animals, plants, and other organisms. Such effects can be mediated by the transmission of epigenetic, cytoplasmic, somatic, nutritional, environmental, and behavioral variation. Building on the work of many authors, we outline a general framework for conceptualizing nongenetic inheritance and its evolutionary implications. This framework shows that, by decoupling phenotypic change from the genotype, nongenetic inheritance can circumvent the limitations of genetic inheritance and thereby influence population dynamics and alter the fitness landscape. The weight of theory and empirical evidence indicates that nongenetic inheritance is a potent factor in evolution that can engender outcomes unanticipated under the Mendelian-genetic model.

Nearly half a century has passed since the discovery of cytoplasmic inheritance of human chloramphenicol resistance. The inheritance was then revealed to take place maternally by mitochondrial DNA (mtDNA). Later, a number of mutations in mtDNA were identified as a cause of severe inheritable metabolic diseases with neurological manifestation, and the impairment of mitochondrial functions has been probed in the pathogenesis of a wide range of illnesses including neurodegenerative diseases. Recently, a growing number of preclinical studies have revealed that animal behaviors are influenced by the impairment of mitochondrial functions and possibly by the loss of mitochondrial stress resilience. Indeed, as high as 54% of patients with one of the most common primary mitochondrial diseases, mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) syndrome, present psychiatric symptoms including cognitive impairment, mood disorder, anxiety, and psychosis. Mitochondria are multifunctional organelles which produce cellular energy and play a major role in other cellular functions including homeostasis, cellular signaling, and gene expression, among others. Mitochondrial functions are observed to be compromised and to become less resilient under continuous stress. Meanwhile, stress and inflammation have been linked to the activation of the tryptophan (Trp)–kynurenine (KYN) metabolic system, which observably contributes to the development of pathological conditions including neurological and psychiatric disorders. This review discusses the functions of mitochondria and the Trp-KYN system, the interaction of the Trp-KYN system with mitochondria, and the current understanding of the involvement of mitochondria and the Trp-KYN system in preclinical and clinical studies of major neurological and psychiatric diseases.

Mammalian fertilization remains a poorly understood event with the vast majority of studies done in the mouse model. The purpose of this review is to revise the current knowledge about semen deposition, sperm transport, sperm capacitation, gamete interactions and early embryonic development with a focus on the porcine model as a relevant, alternative model organism to humans. The review provides a thorough overview of post-ejaculation events inside the sow’s reproductive tract including comparisons with humans and implications for human fertilization and assisted reproductive therapy (ART). Porcine methodology for sperm handling, preservation, in vitro capacitation, oocyte in vitro maturation, in vitro fertilization and intra-cytoplasmic sperm injection that are routinely used in pig research laboratories can be successfully translated into ART to treat human infertility. Last, but not least, new knowledge about mitochondrial inheritance in the pig can provide an insight into human mitochondrial diseases and new knowledge on polyspermy defense mechanisms could contribute to the development of new male contraceptives.

Chloroplasts and mitochondria are subcellular bioenergetic organelles with their own genomes and genetic systems. DNA replication and transmission to daughter organelles produces cytoplasmic inheritance of characters associated with primary events in photosynthesis and respiration. The prokaryotic ancestors of chloroplasts and mitochondria were endosymbionts whose genes became copied to the genomes of their cellular hosts. These copies gave rise to nuclear chromosomal genes that encode cytosolic proteins and precursor proteins that are synthesized in the cytosol for import into the organelle into which the endosymbiont evolved. What accounts for the retention of genes for the complete synthesis within chloroplasts and mitochondria of a tiny minority of their protein subunits? One hypothesis is that expression of genes for protein subunits of energy-transducing enzymes must respond to physical environmental change by means of a direct and unconditional regulatory control—control exerted by change in the redox state of the corresponding gene product. This hypothesis proposes that, to preserve function, an entire redox regulatory system has to be retained within its original membrane-bound compartment. Colocation of gene and gene product for redox regulation of gene expression (CoRR) is a hypothesis in agreement with the results of a variety of experiments designed to test it and which seem to have no other satisfactory explanation. Here, I review evidence relating to CoRR and discuss its development, conclusions, and implications. This overview also identifies predictions concerning the results of experiments that may yet prove the hypothesis to be incorrect.

Symbiotic microbes have become increasingly recognized to mediate interactions between natural enemies and their hosts. The ecologies of these symbioses, however, are poorly understood in many systems, and a predictive framework is needed to guide future studies. To achieve this, we focus on heritable, defensive microbes of insects. Our review of laboratory‐based studies identifies diverse bacterial species that have independently evolved to protect a range of insects against parasitoids, parasites, predators and pathogens. Although defensive mechanisms are typically unknown, some involve toxins or the upregulation of host immunity. Despite substantial benefits of infection in the presence of natural enemies, the protective symbionts of insects are often found at intermediate levels in natural populations. Using a host‐centred population genetics approach made possible by the host restriction and cytoplasmic inheritance of these microbes, we propose that balancing selection plays a major role in symbiont maintenance, with protective benefits in the presence of enemies and infection costs in their absence. Other mediating factors are likely to be important, including temperature, superinfections and transmission dynamics. While few studies have provided evidence for defence in the field, several studies have shown symbiont infection frequencies to be dynamic, varying across temporal and spatial gradients and food–plant associations. Newly presented data from our pea aphid research reveal that temporal shifts in defensive symbiont prevalence can be quite rapid, with Hamiltonella defensa showing 10–20% shifts around a seasonal average of c. 50%. Such findings contrast with more unidirectional changes seen in laboratory population cages, suggesting temporal changes in the costs and benefits of symbionts in the field. To frame future research on defensive symbiont ecology, we briefly consider a range of studies needed to test laboratory‐ and field‐derived predictions on defensive symbiosis. Included are investigations of defensive mechanisms, symbiont‐driven co‐evolution and community‐level effects. We also consider the need for more thorough and highly resolved molecular diagnostics of natural infections, laboratory studies on functional differences between symbiont strains and species and studies on the relative costs and benefits of defenders in nature. The emerging theme of symbiont‐mediated defence across eukaryotes suggests that knowledge of the functional mechanisms behind protection and natural symbiont dynamics could be key to understanding many of the world's antagonistic species interactions. Thus, the development of insects as a model for such studies holds promise for these organisms and beyond.

Maternal effects can play an important role in a diversity of ecological and evolutionary processes such as population dynamics, phenotypic plasticity, niche construction, life-history evolution and the evolutionary response to selection. However, although maternal effects were defined by quantitative geneticists well over half a century ago, there remains some confusion over exactly what phenomena should be characterized as maternal effects and, more importantly, why it matters and how they are defined. We suggest a definition of maternal effects as the causal influence of the maternal genotype or phenotype on the offspring phenotype. This definition differs from some definitions in that it treats maternal effects as a phenomenon, not as a statistical construct. The causal link to maternal genotype or phenotype is the critical component of this definition providing the link between maternal effects and evolutionary and ecological processes. We show why phenomena such as maternal cytoplasmic inheritance and genomic imprinting are distinct genetically from and have different evolutionary consequences than true maternal effects. We also argue that one should consider cases where the maternal effect is conditional on offspring genotype as a class of maternal effects.

[This corrects the article DOI: 10.3389/fpls.2021.713216.].[This corrects the article DOI: 10.3389/fpls.2021.713216.].

Celeriac F 1 hybrid seed production is currently complicated due to the instability of cytoplasmic male sterile lines. To develop alternative alloplasmic CMS lines, an asymmetric protoplast fusion and hybrid screening methodology was established. Celeriac suspension cells protoplasts were used as the acceptor and carrot, coriander and white celery mesophyll protoplasts as the donor for protoplast fusion experiments. Acceptor cytoplasmic inheritance was inhibited by iodoacetamide treatment and donor nuclear genome inheritance was prevented by UV exposure. Protoplasts were selectively stained and fused using electroporation and polyethylene glycol, and candidate hybrid shoots were obtained. One chloroplast and three mitochondrial markers that could distinguish acceptor and donors organelles were used to characterize over 600 plants obtained after fusion events, without identifying any cybrid. In order to increase the testing efficiency a high number of micro plantlets were pooled and hence the presence of the carrot specific Atp1 marker in one of the pooled samples was detected. We demonstrated that fusion took place between celeriac and a carrot indicating that the creation of viable hybrids is possible although at a very low frequency. These findings open the path for new cytoplasmic hybridization and the isolation of novel CMS lines of celeriac.