scholarly journals Mutations in the FIE and MEA Genes That Encode Interacting Polycomb Proteins Cause Parent-of-Origin Effects on Seed Development by Distinct Mechanisms

2000 ◽  
Vol 12 (12) ◽  
pp. 2367-2381 ◽  
Author(s):  
Ramin Yadegari ◽  
Tetsu Kinoshita ◽  
Ofra Lotan ◽  
Gal Cohen ◽  
Anat Katz ◽  
...  
2000 ◽  
Vol 12 (12) ◽  
pp. 2367
Author(s):  
Ramin Yadegari ◽  
Tetsu Kinoshita ◽  
Ofra Lotan ◽  
Gal Cohen ◽  
Anat Katz ◽  
...  

PLoS ONE ◽  
2008 ◽  
Vol 3 (9) ◽  
pp. e3131 ◽  
Author(s):  
Yanchun Li ◽  
Cintia M. Coelho ◽  
Tian Liu ◽  
Song Wu ◽  
Jiasheng Wu ◽  
...  

Development ◽  
2000 ◽  
Vol 127 (11) ◽  
pp. 2493-2502 ◽  
Author(s):  
S. Adams ◽  
R. Vinkenoog ◽  
M. Spielman ◽  
H.G. Dickinson ◽  
R.J. Scott

Some genes in mammals and flowering plants are subject to parental imprinting, a process by which differential epigenetic marks are imposed on male and female gametes so that one set of alleles is silenced on chromosomes contributed by the mother while another is silenced on paternal chromosomes. Therefore, each genome contributes a different set of active alleles to the offspring, which develop abnormally if the parental genome balance is disturbed. In Arabidopsis, seeds inheriting extra maternal genomes show distinctive phenotypes such as low weight and inhibition of mitosis in the endosperm, while extra paternal genomes result in reciprocal phenotypes such as high weight and endosperm overproliferation. DNA methylation is known to be an essential component of the parental imprinting mechanism in mammals, but there is less evidence for this in plants. For the present study, seed development was examined in crosses using a transgenic Arabidopsis line with reduced DNA methylation. Crosses between hypomethylated and wild-type diploid plants produced similar seed phenotypes to crosses between plants with normal methylation but different ploidies. This is consistent with a model in which hypomethylation of one parental genome prevents silencing of alleles that would normally be active only when inherited from the other parent - thus phenocopying the effects of extra genomes. These results suggest an important role for methylation in parent-of-origin effects, and by inference parental imprinting, in plants. The phenotype of biparentally hypomethylated seeds is less extreme than the reciprocal phenotypes of uniparentally hypomethylated seeds. The observation that development is less severely affected if gametes of both sexes (rather than just one) are ‘neutralized’ with respect to parent-of-origin effects supports the hypothesis that parental imprinting is not necessary to regulate development.


2018 ◽  
Author(s):  
Jenn M. Coughlan ◽  
John H. Willis

SummaryRationaleHybrid seed inviability (HSI) is a common reproductive barrier in angiosperms, yet the evolutionary and developmental drivers of HSI remain largely unknown. We test whether conflict between maternal and paternal interests in resource allocation to developing offspring (i.e. parental conflict) are associated with HSI and determine the degree of developmental parallelism between independent incidences of HSI in Mimulus.MethodsWe quantified HSI between M. guttatus and two clades of M. decorus with oppositely asymmetric incompatibilities and surveyed development of hybrid and parental seeds.Key ResultsCrosses between M. guttatus and both clades of M. decorus show parent-of-origin effects on reciprocal F1 seed development, but in opposing directions. Inviable hybrid seeds exhibit paternal excess phenotypes, wherein endosperm is large and chaotic while viable hybrid seeds produce endosperm cells that are smaller and less prolific (i.e. maternal-excess phenotypes).Main ConclusionsWe find strong parent-of-origin effects on development in reciprocal F1s in multiple incidences of HSI in Mimulus. These patterns suggest that parental conflict may be an important force generating HSI in this group, and mismatches between maternal and paternal contributions to developing seeds result in repeatable developmental defects in hybrids.


Author(s):  
Jean-Philippe Vielle-Calzada ◽  
Ueli Grossniklaus ◽  
Charles Spillane

2014 ◽  
Vol 9 (S 01) ◽  
Author(s):  
X Liu ◽  
M Scholz ◽  
A Tönjes ◽  
M Stumvoll ◽  
PF Stadler ◽  
...  

2010 ◽  
Vol 40 (2) ◽  
pp. 111-120 ◽  
Author(s):  
Scott A. Kelly ◽  
Derrick L. Nehrenberg ◽  
Kunjie Hua ◽  
Ryan R. Gordon ◽  
Theodore Garland ◽  
...  

Despite the health-related benefits of exercise, many people do not engage in enough activity to realize the rewards, and little is known regarding the genetic or environmental components that account for this individual variation. We created and phenotyped a large G4 advanced intercross line originating from reciprocal crosses between mice with genetic propensity for increased voluntary exercise (HR line) and the inbred strain C57BL/6J. G4 females (compared to males) ran significantly more when provided access to a running wheel and were smaller with a greater percentage of body fat pre- and postwheel access. Change in body composition resulting from a 6-day exposure to wheels varied between the sexes with females generally regulating energy balance more precisely in the presence of exercise. We observed parent-of-origin effects on most voluntary wheel running and body composition traits, which accounted for 3–13% of the total phenotypic variance pooled across sexes. G4 individuals descended from progenitor (F0) crosses of HR♀ and C57BL/6J♂ ran greater distances, spent more time running, ran at higher maximum speeds/day, and had lower percent body fat and higher percent lean mass than mice descended from reciprocal progenitor crosses (C57BL/6J♀ × HR♂). For some traits, significant interactions between parent of origin and sex were observed. We discuss these results in the context of sex dependent activity and weight loss patterns, the contribution of parent-of-origin effects to predisposition for voluntary exercise, and the genetic (i.e., X-linked or mtDNA variations), epigenetic (i.e., genomic imprinting), and environmental (i.e., in utero environment or maternal care) phenomena potentially modulating these effects.


Diabetes ◽  
2001 ◽  
Vol 50 (12) ◽  
pp. 2850-2857 ◽  
Author(s):  
R. S. Lindsay ◽  
S. Kobes ◽  
W. C. Knowler ◽  
P. H. Bennett ◽  
R. L. Hanson

2007 ◽  
Vol 28 (12) ◽  
pp. 1225-1235 ◽  
Author(s):  
Jason C. Ting ◽  
Elisha D.O. Roberson ◽  
Nathaniel D. Miller ◽  
Alana Lysholm-Bernacchi ◽  
Dietrich A. Stephan ◽  
...  

animal ◽  
2010 ◽  
Vol 4 (5) ◽  
pp. 672-681 ◽  
Author(s):  
N. Neugebauer ◽  
H. Luther ◽  
N. Reinsch

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