Parent-of-origin effectrough endospermmutants in maize

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 screenedrough endosperm(rgh) mutants for parent-of-origin effects using reciprocal crosses with inbred parents. Sixmaternal rough endosperm(mre) and threepaternal rough endosperm(pre) mutants were identified with threemreloci mapped. When inherited from the female parent,mre/+ seeds reduce grain-fill with a rough, etched, or pitted endosperm surface. Pollen transmission ofpremutants results inrghendosperm 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 formre1,mre2, andmre3indicated that the mutant alleles have no bias in transmission. Histological analysis ofmre1,mre2,mre3, andpre*-949showed altered timing of starch grain accumulation and basal endosperm transfer cell layer (BETL) development. Themre1locus delays BETL and starchy endosperm development, whilemre2andpre*-949cause 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.