Progeny Phenotypes Research Articles

Cell Wall Invertases from Maternal Tissues Modulate Sucrose Flux in Apoplastic Pathways During Rice Anther and Seed Development.

Efficient sucrose transport and metabolism are vital for seed and pollen development in plants. Cell wall invertases (CINs) hydrolyze sucrose into glucose and fructose, maintaining a sucrose gradient in the apoplast of sink tissues. In rice, two CIN isoforms, OsCIN1 and OsCIN2, were identified as being specifically expressed in the anthers but not in pollen. Functional analyses through genetic crosses and mutant characterization showed that oscin1/2 double mutants exhibit a sporophytic male-sterile phenotype and produce shrunken seeds. This suggests that CIN activity is essential for proper pollen development and seed formation in rice. Observation of the progeny genotypes and phenotypes from various genetic crosses revealed that the phenotype of oscin1/2 seeds is determined by the genotype of the maternal tissue, indicating the critical role of CIN function in the apoplast between maternal and filial tissues for sucrose transport and metabolism. The CIN activity in the anthers and seeds of wild-type rice was found to be significantly higher-over 500-fold in the anthers and 5-fold in the seeds-than in the leaves, highlighting the importance of CIN in facilitating the efficient unloading of sucrose. These findings suggest that the fine-tuning of CIN activity in the apoplast, achieved through tissue-specific expression and CIN isoform regulation, plays a key role in determining the carbohydrate distribution across different tissues. Understanding this regulatory mechanism could provide opportunities to manipulate carbohydrate allocation to sink organs, potentially enhancing crop yields.

Timing of Maternal Stress Differentially Affects Immune and Stress Phenotypes in Progeny.

Maternal stress during gestation may affect the development and responsiveness of the hypothalamic-pituitary-adrenal axis (HPA) and immune system in the progeny. Stressor type, duration and gestational stage at which the stressor occurs may all influence the short and long-term effects on the future progeny. The present study advances the characterization of the timing of gestational stress on the stress responsiveness and immune and behavioral phenotypes of the progeny. First, parity sows were hand-fed hydrocortisone acetate (stressed) or placebo (controls) during mid or late gestation. Colostrum and cord blood were collected. Blood samples were obtained from a subset of piglets (n = 36) born to these sows during lactation, pre- and post-weaning, and during an ACTH challenge. Stress and immune measures were assessed. Piglets born to sows stressed during mid-gestation had reduced measures of humoral immunity, including immunoglobulins and interleukin-4. Conversely, piglets born to late-stressed sows exhibited a delayed or dampened stress response to weaning and an ACTH challenge. They also had a skewed pro-inflammatory phenotype, as evidenced by increased interleukin-17 and tumor necrosis factor-α. Overall, these data suggest that the stage of gestation at which gestational stress occurs has differential effects on the HPA axis and immune development of the progeny, resulting in differential stress responsiveness and immune and behavioral phenotypes.

Inheritance of summer patch disease tolerance in hard fescue (Festuca brevipila Tracey)

AbstractHard fescue (Festuca brevipila Tracey) is a cool‐season turfgrass known for exceptional performance under low‐maintenance conditions. However, it is susceptible to summer patch disease. Summer patch is a root disease caused by Magnaporthiopsis poae and Magnaporthiopsis meyeri‐festucae. The objective of this study was to investigate the inheritance of summer patch tolerance in controlled crosses of hard fescue. The experimental populations were full‐sib families created by crossing three tolerant and three susceptible parents in a diallel cross. One hundred progeny from each of the 15 crosses and reciprocals were established in a mowed spaced‐plant trial in 2017 (Trial 1) and 2019 (Trial 2). All progeny and selected parental genotypes were arranged in a randomized complete block design with four replications and inoculated with a mixture of an M. meyeri‐festucae isolate (SCR9) and an M. poae isolate (C11). The disease severity of hard fescue genotypes was assessed by visual rating during the summers of 2018, 2019, 2020, and 2021. Variation in disease responses among progeny suggests that inheritance is controlled by a few major genes. The progeny phenotypes were correlated to the parental phenotypes. The estimate of narrow‐sense heritability was 0.20 (± 0.01), while the estimate of broad‐sense heritability was 0.67 (± 0.08). The heritability estimates are modest but indicate the potential for summer patch tolerance to be improved via selection and breeding. This is the first report of heritability estimates for summer patch tolerance in any turf species. This research will help to determine the most efficient selection procedures for summer patch tolerance in hard fescue.

Why not XY? Male monoecious sexual phenotypes challenge the female monoecious paradigm in Cannabis sativa L.

Monoecy in Cannabis sativa L. has long been considered an industrially important trait due to the increased uniformity it offers and was thought to be exclusively associated with XX females. The isolation and characterisation of a monoecious individual with XY chromosomes sourced from non-proprietary germplasm is reported for the first time. The chromosomal make up of this trait was confirmed through inflorescence structure, growth habit, PCR analysis and sexual phenotypes of progeny from a series of targeted crosses. The identification of an XY monoecious phenotype widens our understanding of monoecy in Cannabis and has important implications for breeding, particularly for producing F1-hybrid seed.

Comparison of baseline cataract rates in AB and TL wildtype zebrafish strains

Zebrafish are an outstanding model for assessing the involvement of genes in paediatric cataracts. Gene discovery for cataracts is enhanced by manipulation of the genome of zebrafish embryos and comparing the phenotypes of mutant progeny with the wildtype embryos. However, wildtype laboratory fish can also develop cataracts, potentially confounding the results. In this study, we compared the baseline cataract rate between two commonly used wildtype laboratory strains, AB and TL, and also an outbred transgenic line with mCherry reporter. We assessed a total of 805 lens images of fish at 4 days post-fertilisation for cataracts and scored each cataract observed as mild, moderate or severe. We found that the AB strain had a cataract rate of 16.2%, TL had 8.9%, and mCherry had 0.7% and these rates were significantly different. We found that TL strain had a lower rate of mild cataracts than AB fish, however, the rate of moderate and severe phenotypes in the AB and the TL strain was similar. Overall, we showed that the baseline cataract rate varies significantly between the strains housed in a single facility and conclude that baseline rates of cataracts should be assessed when planning experiments to assess the genetic causes of cataracts.

Prezygotic mate selection is only partially correlated with the expression of NaS-like RNases and affects offspring phenotypes.

Nicotiana attenuata styles preferentially select pollen from among accessions with corresponding expression patterns of NaS-like-RNases (SLRs), and the postpollination ethylene burst (PPEB) is an accurate predictor of seed siring success. However, the ecological consequences of mate selection, its effect on the progeny, and the role of SLRs in the control of ethylene signaling remain unknown. We explored the link between the magnitude of the ethylene burst and expression of the SLRs in a set of recombinant inbred lines (RILs), dissected the genetic underpinnings of mate selection through genome-wide association study (GWAS), and examined its outcome for phenotypes in the next generation. We found that high levels of PPEB are associated with the absence of SLR2 in most of the tested RILs. We identified candidate genes potentially involved in the control of mate selection and showed that pollination of maternal genotypes with their favored pollen donors produces offspring with longer roots. When the maternal genotypes are only able to select against nonfavored pollen donors, the selection for such positive traits is abolished. We conclude that plants' ability of mate choice contributes to measurable changes in progeny phenotypes and is thus likely a target of selection.

148 Does Increased Gametic Variance Translate to Increased Heterogeneity in progeny?

Abstract The expected genetic merit of a new-born calf is simply the average genetic merit estimates of its parents. Parents with a very heterogenous genotype could, however, potentially generate a more heterogenous group of progeny than parents with a more homogenous genotype. The objective of the present study was to test this hypothesis, and a secondary objective was to determine the expected progeny variability in their estimates of genetic merit for traits associated with dairy-beef production based on their expected genomic heterogeneity. Gametic variance for calving difficulty, calf mortality, gestation length, docility, feed intake, and carcass weight, fat, and conformation was estimated for 22,038 beef sires of multiple breeds. Sire gametic variance per trait was estimated for each chromosome from all heterozygous single nucleotide polymorphisms (SNP), their location within the genome, and the estimated effect of each SNP on each trait. Gametic variance was estimated for the whole genome as the sum of the estimated gametic variance of all chromosomes. Individual progeny phenotypic records for each trait were adjusted for animal sex, dam parity and dam genetic merit for the trait, heterosis, recombination loss, and contemporary group. The correlations between sire estimated gametic variance and the standard deviation of his (adjusted) progeny phenotypes were then estimated for all sires with at least 20 progeny records; the number of genotyped sires with at least 20 progeny ranged from 2,395 (heifer calving assistance) to 8,545 (calf mortality). The mean gametic variance, relative to the variance of sire genetic merit, for heifer calving difficulty, cow calving difficulty, calf mortality, gestation length, docility, feed intake, carcass weight, carcass conformation, carcass fat were 0.0002, 0.0005, 0.09, 0.07, 0.30, 0.02, 0.25, 0.05, and 0.12, respectively. With the exception of carcass fat and carcass weight, the correlations between the estimated gametic variance per sire and the standard deviation of his (adjusted) progeny phenotypes were non-existent (-0.06 to 0.04); the correlations between the standard deviation of the adjusted progeny phenotypes and the gametic variance for carcass fat and carcass weight were 0.29 and 0.16, respectively. The (weak) correlations between gametic variance and progeny phenotypes for carcass fat and carcass weight suggest that greater gametic variance is associated with increased progeny heterogeneity for both carcass traits. Nevertheless, accounting for gametic variance when selecting beef bulls for use on dairy females seems to provide little benefit.

Single-Cell Revelation of Extensive Heterogeneity in the Human Lymphocyte and Neutrophil/Monocyte Lineage Restriction Process Despite Highly Co-Regulated Changes in Cell Cycle Control

The production of mature blood lineages in humans has been viewed as a hierarchical process in which the primitive cells with multi-lineage potential generate a series of progenitors with increasingly reduced self-renewal abilities and restricted lineage potentials. This concept has been largely supported by phenotypic characterization of starting CD34+ subsets of human CD45+ cells isolated from different hematopoietic tissues and assayed for their mature cell outputs in supportive systems in vitro or post-transplant and more recently by tracking changes in their molecular composition. Such experiments have suggested that cells that give rise to the lymphocyte lineages (L) share a common origin almost exclusively with the neutrophil and monocyte (macrophage) lineages (NM). However, the mechanisms that regulate the subsequent separation of these lineages starting from cells with presumed restricted L+NM potential have remained elusive. To address this question, we first developed a culture system that supports outputs of differentiated B (CD19+) and NM (CD15+/CD14+) from ≥50% of single CD34+ cells plated on a stromal layer of MS-5 feeders in a medium containing human IL-7, SCF and FLT3L. Use of this clonal assay revealed that cells with B+NM bi-potential constitute 20% of the CD45RA-CLEC12A- (RA-C-) cell subset of the CB “P-Mix” phenotype (CD34+CD38medCD71-CD10-, Blood 133:927, 2019); with the CD45RA+CLEC12A- (RA+C-) and CLEC12A+ (C+) cells displaying largely restricted outputs of only B- (30%) or only NM- (50%) progeny phenotypes, respectively. These same 3 “progenitor” phenotypes (RA-C-, RA+C-, C+) were also found to be regenerated in xenografted immunodeficient mice as well as in a further optimized in vitro system and their clonal output types and numbers consistent with the outputs of those isolated from fresh CB. To analyze T-cell lineage (T) restriction in parallel, we then further modified this culture system to include adherent DLL4, that we found allows B, T, N and M progeny to be produced from single input CB cells at a 40-60% efficiency, with numerous clones derived from single RA+C- cells containing B+T+M, or B+M, or B+T or T-only; a few with B- or M- only, and none with N. In contrast, under the same conditions, half of the documented C+ outputs were exclusively N with much lower lymphoid outputs of T-only or T+N/M. Together, these findings reveal the unanticipated importance of the external stimuli in revealing lineage potentials when these are undergoing restrictive changes. We then asked if and how these identified early phenotypes might change their cycling properties during the course of their progression. For this, the rate and progeny content of sequential cell divisions during the stimulated expansion of the CFSE labelled RA-C- input cells were measured under a supportive liquid culture condition. Throughout a 6-day period, almost all of the C+ progeny and a slightly lower proportion of the RA+C- outputs were generated from cells that transit through the cell cycle within 24 hours, whereas cells maintaining an undifferentiated RA-C- phenotype divided at significantly slower rates, suggesting a simultaneously initiated shortening of the cell cycle transit time during both L- and NM- restriction. In agreement with these functional results, a recent single-cell CITE-seq dataset generated in parallel showed higher expression of genes involved in cycling activities in the early L- and NM-restricted subsets as compared to the unrestricted RA-C- cells. Taken together, these results reveal important and disconnected features in the cell cycle control and previously unrecognized complex patterns in the biological outputs and molecular changes during the steps of L and NM restriction. In addition, they set the stage to enable preferred sequences and molecular changes responsible for normal and regenerative needs to be identified and their potential relevance to the formation of human lymphoblastic and myeloid leukemias to be characterized.

Microevolution of Pseudomonas aeruginosa in the airways of people with cystic fibrosis.

The chronic infections of cystic fibrosis (CF) airways with Pseudomonas aeruginosa are a paradigm of how environmental bacteria can conquer, adapt, and persist in an atypical habitat and successfully evade defense mechanisms and chemotherapy in a susceptible host. The within-host evolution of intraclonal diversity has been examined by whole-genome sequencing, phenotyping, and competitive fitness experiments of serial P. aeruginosa isolates collected from CF airways since onset of colonization for a period of up to 40 years. The spectrum of de novo mutations and the adaptation of phenotype and fitness of the bacterial progeny were more influenced by the living conditions in the CF lung than by the clone type of their ancestor and its genetic repertoire.

Maternal repetitive hypoxia prior to mating confers epigenetic resilience to memory impairment in male progeny.

We showed previously in a mouse model of vascular cognitive impairment and dementia involving chronic cerebral hypoperfusion (CCH) that repetitive hypoxic conditioning (RHC) of both parents results in the epigenetic, intergenerational transmission of resilience to recognition memory loss in adult progeny, as assessed by the novel object recognition test. The present study was undertaken in the same model to determine whether RHC treatment of one or both parents is required to confer dementia resilience intergenerationally. We found inherited resilience to 3 months of CCH in males is maternally mediated (p = .006). Statistically, we observed a strong trend for the paternal germline to contribute as well (p = .052). We also found that, in contrast to what is widely observed in males, females display intact recognition memory (p = .001) after 3 months of CCH, revealing a heretofore unidentified sexual dimorphism with respect to cognitive impact during disease progression. Overall, results of our study strongly implicate epigenetic changes in maternal germ cells, induced by our repetitive systemic hypoxic stimulus, contributing to a modified differentiation program capable of establishing a dementia-resilient phenotype in adult male first-generation progeny. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Boundaries for genotype, phenotype, and pedigree truncation in genomic evaluations in pigs.

Historical data collection for genetic evaluation purposes is a common practice in animal populations; however, the larger the dataset, the higher the computing power needed to perform the analyses. Also, fitting the same model to historical and recent data may be inappropriate. Data truncation can reduce the number of equations to solve, consequently decreasing computing costs; however, the large volume of genotypes is responsible for most of the increase in computations. This study aimed to assess the impact of removing genotypes along with phenotypes and pedigree on the computing performance, reliability, and inflation of GEBV from ssGBLUP for selection candidates. Data from two pig lines, a terminal sire (L1) and a maternal line (L2), were analyzed in this study. Four analyses were implemented: growth and "weaning to finish" mortality on L1, pre-weaning and reproductive traits on L2. Four genotype removal scenarios were proposed: removing genotyped animals without phenotypes and progeny (noInfo), removing genotyped animals based on birth year (Age), the combination of noInfo and Age scenarios (noInfo + Age), and no genotype removal (AllGen). In all scenarios, phenotypes were removed, based on birth year, and three pedigree depths were tested: two and three generations traced back and using the entire pedigree. The full dataset contained 1,452,257 phenotypes for growth traits, 324,397 for weaning to finish mortality, 517,446 for pre-weaning traits, and 7,853,629 for reproductive traits in pure and crossbred pigs. Pedigree files for lines L1 and L2 comprised 3,601,369 and 11,240,865 animals, of which 168,734 and 170,121 were genotyped, respectively. In each truncation scenario, the linear regression method was used to assess the reliability and dispersion of GEBV for genotyped parents (born after 2019). The number of years of data that could be removed without harming reliability depended on the number of records, type of analyses (multitrait vs. single trait), the heritability of the trait, and data structure. All scenarios had similar reliabilities, except for noInfo, which performed better in the growth analysis. Based on the data used in this study, considering the last ten years of phenotypes, tracing three generations back in the pedigree, and removing genotyped animals not contributing own or progeny phenotypes, increases computing efficiency with no change in the ability to predict breeding values.

Reaction-norm analysis of neonatal lamb mortality suggests heritability varies with cold-stress: an example in the Elsenburg Merino selection lines

Context Coping with high levels of cold stress should be beneficial to survival of lambs, given the high mortality rate associated with severe winter storms. The Elsenburg Merino selection experiment involved divergent selection for reproduction. Phenotypic results comparing the positively selected H-Lines and negatively selected L-Lines suggested that cold-stress adaption could have contributed to the favourable genetic trends for survival of H-Line lambs. However, observing the genetic merit of better adapted animals depends on the presence of cold stress at the time of recording. A genotype by environment component (G × E) could, thus, be important when assessing survival/mortality phenotypes. Aim This study proposed the genetic analysis of this possible G × E component and compared the H- and L-Lines in this regard. Methods The sire model allowed the use of progeny phenotypes for neonatal mortality recorded during different levels of cold stress, and the possible G × E could be investigated through the reaction-norm approach. Genetic parameters were evaluated as random regression components by implementing a Gibbs sampling approach. A data set of 5723 individual lamb records was analysed as the progeny of 213 sires. Results A modelled G × E component played an important role in mortality outcomes, with the mean estimate (and 95% confidence interval) for the slope ( σ s b 2 = 0.113 [ 0.0019 – 0.28 ] AN22464_IE1.gif) only marginally smaller than the corresponding estimate for the intercept ( σ s a 2 = 0.124 [ 0.003 – 0.26 ] AN22464_IE2.gif). The reaction-norm model showed a higher heritability (h2 ± posterior standard deviation) for mortality at 3 days of age during high cold-stress (0.22 ± 0.16 at ~1100 KJm−2h−1) than during mild (0.13 ± 0.10 at ~960 KJm−2h−1) conditions, suggesting a greater ability to discriminate between sires at increasing stress levels. Conclusions Failure to account for this G × E component putatively contributes to the low h2 commonly reported for survival traits. The higher h2 at increased levels of cold stress could have played an important part in the higher survival of the H-Line progeny, who were better at coping with cold, wet and windy conditions. Implications Larger studies representing a wider environmental trajectory are recommended. This should be very feasible since cold stress can be derived from commonly available weather-station data.

The vulnerable primed cancer stem cells in disguise: demystifying the role of Maspin.

Epithelial-specific Maspin is widely known as a tumor suppressor. However, while the level of maspin expression is inversely correlated with tumor grade and stage, emerging clinical evidence shows a correlation between seemingly better differentiated tumor cells that express Maspin in both the nucleus and the cytoplasm, (n + c)Maspin, with a poor prognosis of many types of cancer. Biological studies demonstrate that Maspin plays an essential role in stem cell differentiation. In light of the recently established characterization of primed stem cells (P-SCs) in development, we propose, for the first time, that cancer stem cells (CSCs) also need to undergo priming (P-CSCs) before their transition to various progeny phenotypes. We envisage major differences in the steady state kinetics between P-SCs and P-CSCs. We further propose that P-CSCs of carcinoma are both marked and regulated by (n + c)Maspin. The concept of P-CSCs helps explain the apparent dichotomous relationships of (n + c)Maspin expression with cancer diagnosis and prognosis, and is supported by the evidence from mechanistic studies. We believe that the potential utility of (n + c)Maspin as a molecular marker of P-CSCs may significantly accelerate the advancement in our understanding of the genesis of tumor phenotypic plasticity in response to changes of tumor microenvironments (TME) or drug treatments. The vulnerabilities of the cellular state of (n + c)Maspin-expressing P-CSCs are also discussed as the rationale for future development of P-CSC-targeted chemotherapeutic and immunotherapeutic strategies.

Paternal transmission of behavioural and metabolic traits induced by postnatal stress to the 5th generation in mice.

Life experiences and environmental conditions in childhood can change the physiology and behaviour of exposed individuals and, in some cases, of their offspring. In rodent models, stress/trauma, poor diet, and endocrine disruptors in a parent have been shown to cause phenotypes in the direct progeny, suggesting intergenerational inheritance. A few models also examined transmission to further offspring and suggested transgenerational inheritance, but such multigenerational inheritance is not well characterized. Our previous work on a mouse model of early postnatal stress showed that behaviour and metabolism are altered in the offspring of exposed males up to the 4th generation in the patriline and up to the 2nd generation in the matriline. The present study examined if symptoms can be transmitted beyond the 4th generation in the patriline. Analyses of the 5th and 6th generations of mice revealed that altered risk-taking and glucose regulation caused by postnatal stress are still manifested in the 5th generation but are attenuated in the 6th generation. Some of the symptoms are expressed in both males and females, but some are sex-dependent and sometimes opposite. These results indicate that postnatal trauma can affect behaviour and metabolism over many generations, suggesting epigenetic mechanisms of transmission.

Leveraging low-density crossbred genotypes to offset crossbred phenotypes and their impact on purebred predictions.

The objectives of this study were to 1) investigate the predictability and bias of genomic breeding values (GEBV) of purebred (PB) sires for CB performance when CB genotypes imputed from a low-density panel are available, 2) assess if the availability of those CB genotypes can be used to partially offset CB phenotypic recording, and 3) investigate the impact of including imputed CB genotypes in genomic analyses when using the algorithm for proven and young (APY). Two pig populations with up to 207,375 PB and 32,893 CB phenotypic records per trait and 138,026 PB and 32,893 CB genotypes were evaluated. PB sires were genotyped for a 50K panel, whereas CB animals were genotyped for a low-density panel of 600 SNP and imputed to 50K. The predictability and bias of GEBV of PB sires for backfat thickness (BFX) and average daily gain recorded (ADGX) recorded on CB animals were assessed when CB genotypes were available or not in the analyses. In the first set of analyses, direct inverses of the genomic relationship matrix (G) were used with phenotypic datasets truncated at different time points. In the next step, we evaluated the APY algorithm with core compositions differing in the CB genotype contributions. After that, the performance of core compositions was compared with an analysis using a random PB core from a purely PB genomic set. The number of rounds to convergence was recorded for all APY analyses. With the direct inverse of G in the first set of analyses, adding CB genotypes imputed from a low-density panel (600 SNP) did not improve predictability or reduce the bias of PB sires' GEBV for CB performance, even for sires with fewer CB progeny phenotypes in the analysis. That indicates that the inclusion of CB genotypes primarily used for inferring pedigree in commercial farms is of no benefit to offset CB phenotyping. When CB genotypes were incorporated into APY, a random core composition or a core with no CB genotypes reduced bias and the number of rounds to convergence but did not affect predictability. Still, a PB random core composition from a genomic set with only PB genotypes resulted in the highest predictability and the smallest number of rounds to convergence, although bias increased. Genotyping CB individuals for low-density panels is a valuable identification tool for linking CB phenotypes to pedigree; however, the inclusion of those CB genotypes imputed from a low-density panel (600 SNP) might not benefit genomic predictions for PB individuals or offset CB phenotyping for the evaluated CB performance traits. Further studies will help understand the usefulness of those imputed CB genotypes for traits with lower PB-CB genetic correlations and traits not recorded in the PB environment, such as mortality and disease traits.

Molecular programming of the hepatic lipid metabolism via a parental high carbohydrate and low protein diet in rainbow trout

It is now recognised that parental diets could alter their offspring metabolism, concept known as nutritional programming. For agronomic purposes, it has been previously proposed that programming could be employed as a strategy to prepare individual for future nutritional challenges. Concerning cultured fish that belong to high trophic level, plant-derived carbohydrates are a possible substitute for the traditional protein-rich fishmeal in broodstock diet, lowering thus the dietary protein-to-carbohydrate ratio (HC/LP nutrition). However, in mammals, numerous studies have previously demonstrated that parental HC/LP nutrition negatively affects their offspring in the long term. Therefore, the question of possible adaptation to plant-based diets, via parental nutrition, should be explored. First, the maternal HC/LP nutrition induced a global DNA hypomethylation in the liver of their offspring. Interestingly at the gene expression level, the effects brought by the maternal and paternal HC/LP nutrition cumulated in the liver, as indicated by the altered transcriptome. The paternal HC/LP nutrition significantly enhanced cholesterol synthesis at the transcriptomic level. Furthermore, hepatic genes involved in long-chain polyunsaturated fatty acids were significantly increased by the parental HC/LP nutrition, affecting thus both hepatic and muscle fatty acid profiles. Overall, the present study demonstrated that lipid metabolism could be modulated via a parental nutrition in rainbow trout, and that such modulations have consequences on their progeny phenotypes.

Parental methylation mediates how progeny respond to environments of parents and of progeny themselves.

Environments experienced by both parents and offspring influence progeny traits, but the epigenetic mechanisms that regulate the balance of parental vs. progeny control of progeny phenotypes are not known. We tested whether DNA methylation in parents and/or progeny mediates responses to environmental cues experienced in both generations. Using Arabidopsis thaliana, we manipulated parental and progeny DNA methylation both chemically, via 5-azacytidine, and genetically, via mutants of methyltransferase genes, then measured progeny germination responses to simulated canopy shade in parental and progeny generations. We first found that germination of offspring responded to parental but not seed demethylation. We further found that parental demethylation reversed the parental effect of canopy in seeds with low (Cvi-1) to intermediate (Col) dormancy, but it obliterated the parental effect in seeds with high dormancy (Cvi-0). Demethylation did so by either suppressing germination of seeds matured under white-light (Cvi-1) or under canopy (Cvi-0), or by increasing the germination of seeds matured under canopy (Col). Disruption of parental methylation also prevented seeds from responding to their own light environment in one genotype (Cvi-0, most dormant), but it enabled seeds to respond to their own environment in another genotype (Cvi-1, least dormant). Using mutant genotypes, we found that both CG and non-CG DNA methylation were involved in parental effects on seed germination. Parental methylation state influences seed germination more strongly than does the progeny's own methylation state, and it influences how seeds respond to environments of parents and progeny in a genotype-specific manner.

Maternal Microbiota Modulate a Fragile X-like Syndrome in Offspring Mice.

Maternal microbial dysbiosis has been implicated in adverse postnatal health conditions in offspring, such as obesity, cancer, and neurological disorders. We observed that the progeny of mice fed a Westernized diet (WD) with low fiber and extra fat exhibited higher frequencies of stereotypy, hyperactivity, cranial features and lower FMRP protein expression, similar to what is typically observed in Fragile X Syndrome (FXS) in humans. We hypothesized that gut dysbiosis and inflammation during pregnancy influenced the prenatal uterine environment, leading to abnormal phenotypes in offspring. We found that oral in utero supplementation with a beneficial anti-inflammatory probiotic microbe, Lactobacillus reuteri, was sufficient to inhibit FXS-like phenotypes in offspring mice. Cytokine profiles in the pregnant WD females showed that their circulating levels of pro-inflammatory cytokine interleukin (Il)-17 were increased relative to matched gravid mice and to those given supplementary L. reuteri probiotic. To test our hypothesis of prenatal contributions to this neurodevelopmental phenotype, we performed Caesarian (C-section) births using dissimilar foster mothers to eliminate effects of maternal microbiota transferred during vaginal delivery or nursing after birth. We found that foster-reared offspring still displayed a high frequency of these FXS-like features, indicating significant in utero contributions. In contrast, matched foster-reared progeny of L. reuteri-treated mothers did not exhibit the FXS-like typical features, supporting a key role for microbiota during pregnancy. Our findings suggest that diet-induced dysbiosis in the prenatal uterine environment is strongly associated with the incidence of this neurological phenotype in progeny but can be alleviated by addressing gut dysbiosis through probiotic supplementation.

Whole Exome Sequencing-Based Identification of a Novel Gene Involved in Root Hair Development in Barley (Hordeum vulgare L.).

Root hairs play a crucial role in anchoring plants in soil, interaction with microorganisms and nutrient uptake from the rhizosphere. In contrast to Arabidopsis, there is a limited knowledge of root hair morphogenesis in monocots, including barley (Hordeum vulgare L.). We have isolated barley mutant rhp1.e with an abnormal root hair phenotype after chemical mutagenesis of spring cultivar ‘Sebastian’. The development of root hairs was initiated in the mutant but inhibited at the very early stage of tip growth. The length of root hairs reached only 3% of the length of parent cultivar. Using a whole exome sequencing (WES) approach, we identified G1674A mutation in the HORVU1Hr1G077230 gene, located on chromosome 1HL and encoding a cellulose synthase-like C1 protein (HvCSLC1) that might be involved in the xyloglucan (XyG) synthesis in root hairs. The identified mutation led to the retention of the second intron and premature termination of the HvCSLC1 protein. The mutation co-segregated with the abnormal root hair phenotype in the F2 progeny of rhp1.e mutant and its wild-type parent. Additionally, different substitutions in HORVU1Hr1G077230 were found in four other allelic mutants with the same root hair phenotype. Here, we discuss the putative role of HvCSLC1 protein in root hair tube elongation in barley.

All you need to know about sperm RNAs.

Spermatogenesis generates a small and highly specialised type of cell that is apparently incapable of transcription and translation. For many years, this dogma was supported by the assumption that (i) the compact sperm nucleus, resulting from the substitution of histones by protamine during spermatogenesis, renders the genome inaccessible to the transcriptional machinery; and (ii) the loss of most organelles, including endoplasmic reticulum and ribosomes, limits or prevents translational activity. Despite these observations, several types of coding and non-coding RNAs have been identified in human sperm. Their functional roles, particularly during fertilisation and embryonic development, are only now becoming apparent. This review aimed to summarise current knowledge of the origin, types and functional roles of sperm RNAs, and to evaluate the clinical benefits of employing these transcripts as biomarkers of male fertility and reproductive outcomes. The possible contribution of sperm RNAs to intergenerational or transgenerational phenotypic inheritance is also addressed. A comprehensive literature search on PubMed was conducted using the search terms 'sperm' AND 'RNA'. Searches focussed upon articles written in English and published prior to August 2020. The development of more sensitive and accurate RNA technologies, including RNA sequencing, has enabled the identification and characterisation of numerous transcripts in human sperm. Though a majority of these RNAs likely arise during spermatogenesis, other data support an epididymal origin of RNA transmitted to maturing sperm by extracellular vesicles. A minority may also be synthesised by de novo transcription in mature sperm, since a small portion of the sperm genome remains packed by histones. This complex RNA population has important roles in paternal chromatin packaging, sperm maturation and capacitation, fertilisation, early embryogenesis and developmental maintenance. In recent years, additional lines of evidence from animal models support a role for sperm RNAs in intergenerational or transgenerational inheritance, modulating both the genotype and phenotype of progeny. Importantly, several reports indicate that the sperm RNA content of fertile and infertile men differs considerably and is strongly modulated by the environment, lifestyle and pathological states. Transcriptional profiling has considerable potential for the discovery of fertility biomarkers. Understanding the role of sperm transcripts and comparing the sperm RNA fingerprint of fertile and infertile men could help to elucidate the regulatory pathways contributing to male factor infertility. Such data might also provide a molecular explanation for several causes of idiopathic male fertility. Ultimately, transcriptional profiling may be employed to optimise ART procedures and overcome some of the underlying causes of male infertility, ensuring the birth of healthy children.