A cryptic variation in a member of the Ovate Family Proteins is underlying the melon fruit shape QTL fsqs8.1

Key message The gene underlying the melon fruit shape QTL fsqs8.1 is a member of the Ovate Family Proteins. Variation in fruit morphology is caused by changes in gene expression likely due to a cryptic structural variation in this locus. Abstract Melon cultivars have a wide range of fruit morphologies. Quantitative trait loci (QTL) have been identified underlying such diversity. This research focuses on the fruit shape QTL fsqs8.1, previously detected in a cross between the accession PI 124112 (CALC, producing elongated fruit) and the cultivar ‘Piel de Sapo’ (PS, producing oval fruit). The CALC fsqs8.1 allele induced round fruit shape, being responsible for the transgressive segregation for this trait observed in that population. In fact, the introgression line CALC8-1, carrying the fsqs8.1 locus from CALC into the PS genetic background, produced perfect round fruit. Following a map-based cloning approach, we found that the gene underlying fsqs8.1 is a member of the Ovate Family Proteins (OFP), CmOFP13, likely a homologue of AtOFP1 and SlOFP20 from Arabidopsis thaliana and tomato, respectively. The induction of the round shape was due to the higher expression of the CALC allele at the early ovary development stage. The fsqs8.1 locus showed an important structural variation, being CmOFP13 surrounded by two deletions in the CALC genome. The deletions are present at very low frequency in melon germplasm. Deletions and single nucleotide polymorphisms in the fsqs8.1 locus could not be not associated with variation in fruit shape among different melon accessions, what indicates that other genetic factors should be involved to induce the CALC fsqs8.1 allele effects. Therefore, fsqs8.1 is an example of a cryptic variation that alters gene expression, likely due to structural variation, resulting in phenotypic changes in melon fruit morphology.

Widespread cryptic variation in genetic architecture between the sexes

The majority of the genome is shared between the sexes, and it is expected that the genetic architecture of most traits is shared as well. This common architecture has been viewed as a major source of constraint on the evolution of sexual dimorphism (SD). SD is nonetheless common in nature, leading to assumptions that it results from differential regulation of shared genetic architecture. Here, we study the effect of thousands of gene knock-out mutations on 202 mouse phenotypes to explore how regulatory variation affects SD. We show that many traits are dimorphic to some extent, and that a surprising proportion of knock-outs have sex-specific phenotypic effects. Many traits, regardless whether they are monomorphic or dimorphic, harbor cryptic differences in genetic architecture between the sexes, resulting in sexually discordant phenotypic effects from sexually concordant regulatory changes. This provides an alternative route to dimorphism through sex-specific genetic architecture, rather than differential regulation of shared architecture.

Adaptive and non-adaptive plasticity in changing environments: implications for sexual species with different life history strategies

Populations adapt to novel environmental conditions by genetic changes or phenotypic plasticity. Plastic responses are generally faster and can buffer fitness losses under variable conditions. Plasticity is typically modelled as random noise and linear reaction norms that assume simple one-to-one genotype-phenotype maps and no limits to the phenotypic response. Most studies on plasticity have focused on its effect on population viability. However, it is not clear, whether the advantage of plasticity depends solely on environmental fluctuations or also on the genetic and demographic properties (life histories) of populations. Here we present an individual-based model and study the relative importance of adaptive and non-adaptive plasticity for populations of sexual species with different life histories experiencing directional stochastic climate change. Environmental fluctuations were simulated using differentially autocorrelated climatic stochasticity or noise color, and scenarios of directional climate change. Non-adaptive plasticity was simulated as a random environmental effect on trait development, while adaptive plasticity as a linear, logistic, or sinusoidal reaction norm. The last two imposed limits to the plastic response and emphasized flexible interactions of the genotype with the environment. Interestingly, this assumption led to (i) smaller phenotypic than genotypic variance in the population and the coexistence of polymorphisms, (ii) many-to-one genotype-phenotype map, and (iii) the maintenance of higher genetic variation – compared to linear reaction norms and genetic determinism – even when the population was exposed to a constant environment for several generations. Limits to plasticity led to genetic accommodation, when costs were negligible, and to the appearance of cryptic variation when limits were exceeded. We found that adaptive plasticity promoted population persistence under red noise stochasticity and was particularly important for life histories with low fecundity. Populations producing more offspring could cope with environmental fluctuations solely by genetic changes or random plasticity, unless environmental change was too fast.

Investigation of the Piroplasm Diversity Circulating in Wildlife and Cattle of the Greater Kafue Ecosystem, Zambia

Background: Piroplasms are vector-borne intracellular haemoprotozoan parasites that infect wildlife and livestock. Wildlife species are reservoir hosts to a diversity of piroplasms and play an important role in the circulation, maintenance and evolution of these parasites. The potential for likely spillover of both pathogenic and non-pathogenic piroplasms from wildlife to livestock is underlined when common ecological niche is shared in the presence of a competent vector. Method: To investigate piroplasm cryptic variation and diversity in parasite community in wildlife and cattle population of the greater Kafue ecosystem, we utilized PCR to amplify the 18S rRNA V4 hyper-variable region and meta-barcoding strategy using illumina MiSeq sequencing platform and amplicon sequence variant (ASV) based bioinformatics pipeline to generate high resolution data which discriminate sequences down to a single nucleotide difference. Results: A parasite community of 45 ASVs and 23 piroplasm species consisting of 4 genera of Babesia, Theileria, Hepatozoon and Colpodella was identified in wildlife and cattle population from the study area. Conclusion: The findings of this study demonstrates the usefulness of illumina MiSeq sequencing to describe the area specific parasite composition, which is critical in the application and establishment of disease control strategy options of ideal diagnostic tools to employ and area specific vaccine development.

Natural cryptic variation in epigenetic modulation of an embryonic gene regulatory network

Gene regulatory networks (GRNs) that direct animal embryogenesis must respond to varying environmental and physiological conditions to ensure robust construction of organ systems. While GRNs are evolutionarily modified by natural genomic variation, the roles of epigenetic processes in shaping plasticity of GRN architecture are not well understood. The endoderm GRN inCaenorhabditis elegansis initiated by the maternally supplied SKN-1/Nrf2 bZIP transcription factor; however, the requirement for SKN-1 in endoderm specification varies widely among distinctC. eleganswild isotypes, owing to rapid developmental system drift driven by accumulation of cryptic genetic variants. We report here that heritable epigenetic factors that are stimulated by transient developmental diapause also underlie cryptic variation in the requirement for SKN-1 in endoderm development. This epigenetic memory is inherited from the maternal germline, apparently through a nuclear, rather than cytoplasmic, signal, resulting in a parent-of-origin effect (POE), in which the phenotype of the progeny resembles that of the maternal founder. The occurrence and persistence of POE varies between different parental pairs, perduring for at least 10 generations in one pair. This long-perduring POE requires piwi-interacting RNA (piRNA) function and the germline nuclear RNA interference (RNAi) pathway, as well as MET-2 and SET-32, which direct histone H3K9 trimethylation and drive heritable epigenetic modification. Such nongenetic cryptic variation may provide a resource of additional phenotypic diversity through which adaptation may facilitate evolutionary changes and shape developmental regulatory systems.

Cryptic diversity in the model fern genus Ceratopteris (Pteridaceae)

Cryptic species are present throughout the tree of life. They are especially prevalent in ferns, because of processes such hybridization, polyploidy, and reticulate evolution. In addition, the morphological simple body plan of ferns limits phenotypic variation and makes it difficult to detect crypic species in ferns without molecular work. The model fern genus Ceratopteris has long been suspected to harbor cryptic diversity, specifically in the highly polymorphic C. thalictroides. Yet no studies have included samples from throughout the pan-tropical range of Ceratopteris or utilized genomic sequencing, making it difficult to assess the full extent of cryptic variation within this genus. Here, we present the first multilocus phylogeny of the genus using reduced representation genomic sequencing (RADseq) and examine population structure, phylogenetic relationships, and ploidy level variation. We recover similar species relationships found in previous studies, find support for a named cryptic species as genetically distinct, and identify a novel putative species from within C. thalictroides sensu latu in Central and South America.