Parent-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-oforigin 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 mutants 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.KEYWORDS parent-of-origin effect; gametophyte; imprinting; seed; endosperm T HE maternal and paternal parents have different genetic and epigenetic contributions to angiosperm seed development. Angiosperm seeds result from the double fertilization of two multicellular gametophytes (Walbot and Evans 2003). In diploid species, gametophytes grow from the haploid products of meiosis with the male and female gametophytes following different developmental programs. The male gametophyte or pollen grain, delivers two haploid sperm cells through the pollen tube to fertilize the female gametophyte. Fertilization of the egg forms a diploid zygote, and fertilization of the two central cell nuclei forms a triploid endosperm cell. The central cell and egg cell provide the vast majority of cytoplasm for the nascent endosperm and the zygote. In addition, the central cell genome has more open chromatin, and there is substantial evidence for a dominant maternal role to initiate the coordinate development of the endosperm and embryo (Baroux and Autran 2015;Borg and Borg 2015;Del Toro-De Leon et al. 2016).Mutations in loci specific to the development of either gametophyte are expected to show non-Mendelian inheritance such as reduced transmission and maternal effect seed phenotypes. Only a few maize seed mutants have been identified with maternal effects, and most of these mutants primarily affect gametophyte development. T...

Parent-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-oforigin 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 mutants 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.KEYWORDS parent-of-origin effect; gametophyte; imprinting; seed; endosperm T HE maternal and paternal parents have different genetic and epigenetic contributions to angiosperm seed development. Angiosperm seeds result from the double fertilization of two multicellular gametophytes (Walbot and Evans 2003). In diploid species, gametophytes grow from the haploid products of meiosis with the male and female gametophytes following different developmental programs. The male gametophyte or pollen grain, delivers two haploid sperm cells through the pollen tube to fertilize the female gametophyte. Fertilization of the egg forms a diploid zygote, and fertilization of the two central cell nuclei forms a triploid endosperm cell. The central cell and egg cell provide the vast majority of cytoplasm for the nascent endosperm and the zygote. In addition, the central cell genome has more open chromatin, and there is substantial evidence for a dominant maternal role to initiate the coordinate development of the endosperm and embryo (Baroux and Autran 2015;Borg and Borg 2015;Del Toro-De Leon et al. 2016).Mutations in loci specific to the development of either gametophyte are expected to show non-Mendelian inheritance such as reduced transmission and maternal effect seed phenotypes. Only a few maize seed mutants have been identified with maternal effects, and most of these mutants primarily affect gametophyte development. T...