scholarly journals Parent-of-origin effect rough endosperm mutants in maize

2016 ◽  
Author(s):  
Fang Bai ◽  
Mary Daliberti ◽  
Alyssa Bagadion ◽  
Miaoyun Xu ◽  
Yubing Li ◽  
...  
Keyword(s):  
Female Parent ◽  
Mendelian Inheritance ◽  
Endosperm Development ◽  
Paternal Allele ◽  
Imprinted Genes ◽  
Incomplete Penetrance ◽  
Starchy Endosperm ◽  
Parent Of Origin ◽  
Origin Effects ◽  
Origin Effect

ABSTRACTParent-of-origin effect loci have non-Mendelian inheritance in which phenotypes are determined by either the maternal or paternal allele alone. In angiosperms, parent-of-origin effects can be caused by loci required for gametophyte development or by imprinted genes needed for seed development. Few parent-of-origin effect loci have been identified in maize (Zea mays) even though there are a large number of imprinted genes known from transcriptomics. We screened rough endosperm (rgh) mutants for parent-of-origin effects using reciprocal crosses with inbred parents. Six maternal rough endosperm (mre) and three paternal rough endosperm (pre) mutants were identified with three mre loci mapped. When inherited from the female parent, mre/+ seeds reduce grain-fill with a rough, etched, or pitted endosperm surface. Pollen transmission of pre mutants results in rgh endosperm as well as embryo lethality. Eight of the loci had significant distortion from the expected one-to-one ratio for parent-of-origin effects. Linked markers for mre1, mre2, and mre3 indicated that the mutant alleles have no bias in transmission. Histological analysis of mre1, mre2, mre3, and pre*-949 showed altered timing of starch grain accumulation and basal endosperm transfer cell layer (BETL) development. The mre1 locus delays BETL and starchy endosperm development, while mre2 and pre*-949 cause ectopic starchy endosperm differentiation. We conclude that many parent-of-origin effects in maize have incomplete penetrance of kernel phenotypes and that there is a large diversity of endosperm developmental roles for parent-of-origin effect loci.

scholarly journals Lack of parent-of-origin effects in Nasonia jewel wasp: A replication and extension study

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0252457
Author(s):  
Kimberly C. Olney ◽  
Joshua D. Gibson ◽  
Heini M. Natri ◽  
Avery Underwood ◽  
Juergen Gadau ◽  
...  
Keyword(s):  
Genomic Imprinting ◽  
Sequence Data ◽  
Original Data ◽  
Paternal Allele ◽  
Analysis Strategy ◽  
Parent Of Origin ◽  
Origin Effects ◽  
New Processing ◽  
Diploid Cells ◽  
Origin Effect

In diploid cells, the paternal and maternal alleles are, on average, equally expressed. There are exceptions from this: a small number of genes express the maternal or paternal allele copy exclusively. This phenomenon, known as genomic imprinting, is common among eutherian mammals and some plant species; however, genomic imprinting in species with haplodiploid sex determination is not well characterized. Previous work reported no parent-of-origin effects in the hybrids of closely related haplodiploid Nasonia vitripennis and Nasonia giraulti jewel wasps, suggesting a lack of epigenetic reprogramming during embryogenesis in these species. Here, we replicate the gene expression dataset and observations using different individuals and sequencing technology, as well as reproduce these findings using the previously published RNA sequence data following our data analysis strategy. The major difference from the previous dataset is that they used an introgression strain as one of the parents and we found several loci that resisted introgression in that strain. Our results from both datasets demonstrate a species-of-origin effect, rather than a parent-of-origin effect. We present a reproducible workflow that others may use for replicating the results. Overall, we reproduced the original report of no parent-of-origin effects in the haplodiploid Nasonia using the original data with our new processing and analysis pipeline and replicated these results with our newly generated data.

scholarly journals Lack of parent-of-origin effects in Nasonia jewel wasp: a replication and extension study

2021 ◽  
Author(s):  
Kimberly C. Olney ◽  
Joshua D. Gibson ◽  
Heini M. Natri ◽  
Avery Underwood ◽  
Juergen Gadau ◽  
...  
Keyword(s):  
Genomic Imprinting ◽  
Sequence Data ◽  
Original Data ◽  
Paternal Allele ◽  
Analysis Strategy ◽  
Parent Of Origin ◽  
Origin Effects ◽  
New Processing ◽  
Diploid Cells ◽  
Origin Effect

AbstractIn diploid cells, the paternal and maternal alleles are, on average, equally expressed. There are exceptions from this: a small number of genes express the maternal or paternal allele copy exclusively. This phenomenon, known as genomic imprinting, is common among eutherian mammals and some plant species; however, genomic imprinting in species with haplodiploid sex determination is not well characterized. Previous work reported no parent-of-origin effects in the hybrids of closely related haplodiploid Nasonia vitripennis and Nasonia giraulti jewel wasps, suggesting a lack of epigenetic reprogramming during embryogenesis in these species. Here, we replicate the gene expression dataset and observations using different individuals and sequencing technology, as well as reproduce these findings using the previously published RNA sequence data following our data analysis strategy. The major difference from the previous dataset is that they used an introgression strain as one of the parents and we found several loci that resisted introgression in that strain. Our results from both datasets demonstrate a species-of-origin effect, rather than a parent-of-origin effect. We present a reproducible workflow that others may use for replicating the results. Overall, we reproduced the original report of no parent-of-origin effects in the haplodiploid Nasonia using the original data with our new processing and analysis pipeline and replicated these results with our newly generated data.

scholarly journals Parent-of-origin effects on cardiac response to pressure overload in mice

2009 ◽  
Vol 297 (3) ◽  
pp. H1003-H1009 ◽  
Author(s):  
Cordelia J. Barrick ◽  
Anping Dong ◽  
Rebekah Waikel ◽  
Drew Corn ◽  
Fanmuyi Yang ◽  
...  
Keyword(s):  
Y Chromosome ◽  
Pressure Overload ◽  
Inbred Strains ◽  
Mendelian Inheritance ◽  
Left Ventricular ◽  
Cardiac Response ◽  
Heart Weight ◽  
Parental Origin ◽  
Parent Of Origin ◽  
Origin Effects

Left ventricular (LV) hypertrophy (LVH) is an independent risk factor for cardiovascular mortality and is commonly caused by hypertension. In rodents, transverse aortic constriction (TAC) is a model regularly employed in mechanistic studies of the response of the LV to pressure overload. We previously reported that inbred strains of male mice manifest different cardiac responses to TAC, with C57BL/6J (B6) developing LV dilatation and impaired contractility and 129S1/SvImJ (129) males displaying concentric LVH. In the present study, we investigated sex and parent-of-origin effects on the response to TAC by comparing cardiac function, organ weights, expression of cardiac hypertrophy markers, and histology in female B6 and female 129 mice and in F1 progeny of reciprocal crosses between B6 and 129 mice (B6129F1 and 129B6F1). Five weeks after TAC, heart weight increased to the greatest extent in 129B6F1 mice and the least extent in 129 and B6129F1 mice. Female 129B6F1 and B6 mice were relatively protected from the increase in heart weight that occurs in their male counterparts with pressure overload. The response to TAC in 129 consomic mice bearing the B6 Y chromosome resembled that of 129 rather than 129B6F1 mice, indicating that the B6 Y chromosome does not account for the differences in the reciprocal cross. Our results suggest that susceptibility to LVH is more complex than simple Mendelian inheritance and that parental origin effects strongly impact the LV response to TAC in these commonly used inbred strains.

scholarly journals Epistatic Networks Associated with Parent-of-Origin Effects on Metabolic Traits

2019 ◽  
Author(s):  
Juan F Macias-Velasco ◽  
Celine L. St. Pierre ◽  
Jessica P Wayhart ◽  
Li Yin ◽  
Larry Spears ◽  
...  
Keyword(s):  
Complex Traits ◽  
Reciprocal Cross ◽  
Expression Profiles ◽  
Specific Interaction ◽  
Imprinted Genes ◽  
Cross Model ◽  
Metabolic Traits ◽  
Parent Of Origin ◽  
Origin Effects ◽  
Context Specific

ABSTRACTParent-of-origin effects (POE) are unexpectedly common in complex traits, including metabolic and neurological diseases. POE can also be modified by the environment, but the architecture of these gene-by-environmental effects on phenotypes remains to be unraveled. Previously, quantitative trait loci (QTL) showing context-specific POE on metabolic traits were mapped in the F16 generation of an advanced intercross between LG/J and SM/J inbred mice. However, these QTL were not enriched for known imprinted genes, suggesting another mechanism is needed to explain these POE phenomena. Here, we use a simple yet powerful F1 reciprocal cross model to test the hypothesis that non-imprinted genes can generate complex POE on metabolic traits through genetic interactions with imprinted genes. Male and female mice from a F1 reciprocal cross of LG/J and SM/J strains were fed either high or low fat diets. We generated expression profiles from three metabolically-relevant tissues: hypothalamus, white adipose, and liver. We identified two classes of parent-of-origin expression biases: genes showing parent-of-origin-dependent allele-specific expression and biallelic genes that are differentially expressed by reciprocal cross. POE patterns of both gene classes are highly tissue-and context-specific, sometimes occurring only in one sex and/or diet cohort in a particular tissue. We then constructed tissue-specific interaction networks among genes from these two classes of POE. A key subset of gene pairs show significant epistasis in the F16 LG/J x SM/J advanced intercross data in cases where the biallelic gene fell within a previously-identified metabolic POE QTL interval. We highlight one such interaction in adipose, between Nnat and Mogat1, which associates with POE on multiple adiposity traits. Both genes localize to the endoplasmic reticulum of adipocytes and play a role in adipogenesis. Additionally, expression of both genes is significantly correlated in human visceral adipose tissue. The genes and networks we present here represent a set of actionable interacting candidates that can be probed to further identify the machinery driving POE on complex traits.

scholarly journals Parent-of-origin effects propagate through networks to shape metabolic traits

2021 ◽  
Author(s):  
Juan F Macias-Velasco ◽  
Celine L. St. Pierre ◽  
Jessica P Wayhart ◽  
Li Yin ◽  
Larry Spears ◽  
...  
Keyword(s):  
Complex Traits ◽  
Neurological Diseases ◽  
Inbred Mice ◽  
Inbred Mouse ◽  
Serum Glucose ◽  
Physiological Data ◽  
Imprinted Genes ◽  
Metabolic Traits ◽  
Parent Of Origin ◽  
Origin Effects

ABSTRACTParent-of-origin effects are unexpectedly common in complex traits, including metabolic and neurological diseases. Parent-of-origin effects can be modified by the environment, but the architecture of these gene-by-environmental effects on phenotypes remains to be unraveled. Previously, quantitative trait loci (QTL) showing context-specific parent-of-origin effects on metabolic traits were mapped in the F16 generation of an advanced intercross between LG/J and SM/J inbred mice. However, these QTL were not enriched for known imprinted genes, suggesting another mechanism is needed to explain these parent-of-origin effects phenomena. We propose that non-imprinted genes can generate complex parent-of-origin effects on metabolic traits through interactions with imprinted genes. Here, we employ data from mouse populations at different levels of intercrossing (F0, F1, F2, F16) of the LG/J and SM/J inbred mouse lines to test this hypothesis. Using multiple populations and incorporating genetic, genomic, and physiological data, we leverage orthogonal evidence to identify networks of genes through which parent-of-origin effects propagate. We identify a network comprised of 3 imprinted and 6 non-imprinted genes that show parent-of-origin effects. This epistatic network forms a nutritional responsive pathway and the genes comprising it jointly serve cellular functions associated with growth. We focus on 2 genes, Nnat and F2r, whose interaction associates with serum glucose levels across generations in high fat-fed females. Single-cell RNAseq reveals that Nnat and F2r are negatively correlated in pre-adipocytes along an adipogenic trajectory, a result that is consistent with our observations in bulk white adipose tissue.

scholarly journals A parent-of-origin effect on honeybee worker ovary size

2014 ◽  
Vol 281 (1775) ◽  
pp. 20132388 ◽  
Author(s):  
Benjamin P. Oldroyd ◽  
Michael H. Allsopp ◽  
Katherine M. Roth ◽  
Emily J. Remnant ◽  
Robert A. Drewell ◽  
...  
Keyword(s):  
Apis Mellifera ◽  
Reproductive Traits ◽  
Female Offspring ◽  
Apis Mellifera Capensis ◽  
Intragenomic Conflict ◽  
Size Number ◽  
Parent Of Origin ◽  
Origin Effects ◽  
Honeybee Subspecies ◽  
Origin Effect

Apis mellifera capensis is unique among honeybees in that unmated workers can produce pseudo-clonal female offspring via thelytokous parthenogenesis. Workers use this ability to compete among themselves and with their queen to be the mother of new queens. Males could therefore enhance their reproductive success by imprinting genes that enhance fertility in their daughter workers. This possibility sets the scene for intragenomic conflict between queens and drones over worker reproductive traits. Here, we show a strong parent-of-origin effect for ovary size (number of ovarioles) in reciprocal crosses between two honeybee subspecies, A. m. capensis and Apis mellifera scutellata. In this cross, workers with an A. m. capensis father had 30% more ovarioles than genotypically matched workers with an A. m. scutellata father. Other traits we measured (worker weight at emergence and the presence/absence of a spermatheca) are influenced more by rearing conditions than by parent-of-origin effects. Our study is the first to show a strong epigenetic (or, less likely, cytoplasmic maternal) effect for a reproductive trait in the honeybee and suggests that a search for parent-of-origin effects in other social insects may be fruitful.

scholarly journals Imprinted Genes and Multiple Sclerosis: What Do We Know?

2021 ◽  
Vol 22 (3) ◽  
pp. 1346
Author(s):  
Natalia Baulina ◽  
Ivan Kiselev ◽  
Olga Favorova
Keyword(s):  
Gene Expression ◽  
Multiple Sclerosis ◽  
Molecular Mechanisms ◽  
Imprinted Genes ◽  
Factors Affecting ◽  
Phenotypic Differences ◽  
The Central Nervous System ◽  
Parent Of Origin ◽  
Origin Effects

Multiple sclerosis (MS) is a chronic autoimmune neurodegenerative disease of the central nervous system that arises from interplay between non-genetic and genetic risk factors. The epigenetics functions as a link between these factors, affecting gene expression in response to external influence, and therefore should be extensively studied to improve the knowledge of MS molecular mechanisms. Among others, the epigenetic mechanisms underlie the establishment of parent-of-origin effects that appear as phenotypic differences depending on whether the allele was inherited from the mother or father. The most well described manifestation of parent-of-origin effects is genomic imprinting that causes monoallelic gene expression. It becomes more obvious that disturbances in imprinted genes at the least affecting their expression do occur in MS and may be involved in its pathogenesis. In this review we will focus on the potential role of imprinted genes in MS pathogenesis.

Analysis of parent of origin effects in Sorbs using long range phasing algorithms

2014 ◽  
Vol 9 (S 01) ◽  
Author(s):  
X Liu ◽  
M Scholz ◽  
A Tönjes ◽  
M Stumvoll ◽  
PF Stadler ◽  
...  
Keyword(s):  
Long Range ◽  
Parent Of Origin ◽  
Origin Effects

scholarly journals Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Laura Santini ◽  
Florian Halbritter ◽  
Fabian Titz-Teixeira ◽  
Toru Suzuki ◽  
Maki Asami ◽  
...  
Keyword(s):  
Bisulfite Sequencing ◽  
Blastocyst Stage ◽  
Preimplantation Embryos ◽  
Imprinted Genes ◽  
Specific Expression ◽  
Histone 3 ◽  
Complex Program ◽  
Genome Bisulfite Sequencing ◽  
Mammalian Genomes ◽  
Parent Of Origin

AbstractIn mammalian genomes, differentially methylated regions (DMRs) and histone marks including trimethylation of histone 3 lysine 27 (H3K27me3) at imprinted genes are asymmetrically inherited to control parentally-biased gene expression. However, neither parent-of-origin-specific transcription nor imprints have been comprehensively mapped at the blastocyst stage of preimplantation development. Here, we address this by integrating transcriptomic and epigenomic approaches in mouse preimplantation embryos. We find that seventy-one genes exhibit previously unreported parent-of-origin-specific expression in blastocysts (nBiX: novel blastocyst-imprinted expressed). Uniparental expression of nBiX genes disappears soon after implantation. Micro-whole-genome bisulfite sequencing (µWGBS) of individual uniparental blastocysts detects 859 DMRs. We further find that 16% of nBiX genes are associated with a DMR, whereas most are associated with parentally-biased H3K27me3, suggesting a role for Polycomb-mediated imprinting in blastocysts. nBiX genes are clustered: five clusters contained at least one published imprinted gene, and five clusters exclusively contained nBiX genes. These data suggest that early development undergoes a complex program of stage-specific imprinting involving different tiers of regulation.

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