Maternal effects in plants were recognized as long ago as 1909 (32). Recent evidence, primarily over the last 15-20 years, shows that maternal effects can contribute substantially to the phenotype of an individual, and as we show, this has important consequences for the interpretation and' design of both ecofogical and genetic studies. Following a discussion of the consequences of maternal effects and an analysis of the different ways these effects can be estimated, we review the evidence for maternal effects from the fields of physiological ecology, crop science, and quantitative genetics. We do not review all of the literature because that would be a monumental task; rather, we focus on representative studies from each of these fields. It is our contention that despite evidence that maternal effects can have a large in­ fluence on offspring phenotype, few detailed studies have identified the specific causes of maternal effects, particularly in natural populations.

Maternal effects in plants

Apart from their agronomic importance in hybrid seed production, mutations that encode cytoplasmic male sterility (CMS) provide a means to probe the role of the mitochondrion in reproductive development. Fertility restorers are examples of nuclear genes that affect cytoplasmic gene expression, and

Interactions of Mitochondrial and Nuclear Genes That Affect Male Gametophyte Development

The T cytoplasm of maize serves as a model for the nuclear restoration of cytoplasmic male sterility. The rf2 gene, one of two nuclear genes required for fertility restoration in male-sterile T-cytoplasm (cmsT) maize, was cloned. The protein predicted by the rf2 sequence is a putative aldehyde dehydrogenase, which suggests several mechanisms that might explain Rf2-mediated fertility restoration in cmsT maize. Aldehyde dehydrogenase may be involved in the detoxification of acetaldehyde produced by ethanolic fermentation during pollen development, may play a role in energy metabolism, or may interact with URF13, the mitochondrial protein associated with male sterility in cmsT maize.

https://schnablelab.plantgenomics.iastate.edu/docs/research/publications/Science_vol272pp1334.pdf

The rf2 nuclear restorer gene of male-sterile T-cytoplasm maize.

Cytoplasmic male sterility (CMS) is the maternal transmission of failed pollen production in hermaphroditic plants leading to a mixture of male-sterile and hermaphroditic individuals in the population (gynodioecy). Autosomal genes that can restore pollen fertility in the presence of male-sterile cytotypes are commonly observed. CMS in wild populations tends to be associated with (1) the maintenance of distinct cytotypes, each capable of causing male sterility by an apparently different mechanism since each is susceptible to only a particular subset of autosomal restorer alleles; (2) the maintenance of polymorphism at several autosomal restorer loci, with particular alleles or loci specialized for restoring pollen fertility when associated with particular cytotypes; (3) the maintenance of genetic differentiation among geographically distant populations; and (4) the maintenance of phenotypic diversity among populations, measured as the percentage of malesterile individuals. Observations and previous theoret...

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The Evolutionary Dynamics of Cytoplasmic Male Sterility

A fused mitochondrial gene associated with cytoplasmic male sterility is developmentally regulated.

Publisher Summary The generality of cytoplasmic male sterility (CMS) suggests that understanding its basis may give the fundamental information about cytoplasmic genomes functioning in plant development. This chapter describes the male sterility in Petunia, maize, sorghum, sugarbeet, Nicotiana, Vicia faba, sunflower, Solanum, cruciferous species, pearl millet, carrot, wheat and rye, and barley. In some CMS systems, identification of a CMS-specific DNA sequence and its products may immediately reveal why microspores or male reproductive tissues do not develop properly. However, mere identification of a CMS-correlated gene and protein of unknown function would not reveal the mechanism of CMS without further cytological, biochemical, and physiological studies. As functions of mitochondrial-encoded polypeptides have become known, new models for CMS mechanisms may arise. Such models could most readily be tested if cloned Mitochondrial DNA (mtDNA) sequences could be introduced anew into mitochondrial genomes. The underlying mechanisms of CMS are likely to be as diverse as the abnormal reproductive phenotypes observed within and among species.

Mary F. Conde

Papers

Functioning and Variation of Cytoplasmic Genomes: Lessons from Cytoplasmic–Nuclear Interactions Affecting Male Fertility in Plants