Two cytoplasmic male sterility phenotypes in beet (Beta vulgaris L.): implications of their simultaneous onset and divergent paths

Abstract

Cytoplasmic male sterility (CMS) is a mitochondrion-encoded trait specifically affecting anthers. Several male sterility-inducing mitochondrial types are known, many of which affect the development of anther tapetum cells, but no sound explanation for this tissue's vulnerability has been proposed. Insights into the cause of CMS can be obtained by the detailed phenotypic comparison of different male sterility-inducing mitochondrial types of the same plant species. In pursuit of this objective, we conducted an investigation into anther development in two sugar beet CMS lines. We compared an Owen type CMS line used for hybrid breeding with the G type CMS line derived from wild beet. Both CMS lines have the same nuclear background. The tapetum of the G CMS line exhibited hypertrophy in the microspore stage, as reported previously in Owen CMS lines. Ultrastructural analysis revealed mitochondrial abnormalities, including low electron density and aberrant cristae appearing in the tapetum after meiosis in both lines. The Owen CMS line lacked Ubisch bodies and had poorly developed bacula and tecta in the pollen cell walls, whereas the G CMS line retained these features, but the pollen wall was highly deformed. Ultimately, microspores and the tapetum degenerated in both lines, and the male sterile phenotypes were eventually very similar. Although it had been hypothesized that mitochondrial activation was associated with CMS expression, mitochondria in the root apical meristem appeared normal in beet roots with G- and Owen type mitochondria. We propose that CMS expression includes at least two mechanisms: one triggers abnormal mitochondrial generation, and the other affects the type of developmental abnormality.