Triticeae Genomics and Genetics
TGG 2010, Vol.1, No.1
http://tgg.sophiapublisher.com
Page 6 of 7
nucleus-mitochondrion
incompatibility.
Thus,
mitochondrial mutations induce abnormal anther
development and the CMS trait occurred. The
introduction of nuclear restorer gene(s) from restorer
line 5253 reversed the changes caused to the
mitochondrial genome thereby resulting in fertile F1
hybrids. The results confirmed the mtDNA variation
among Aegilops species, CMS lines and their
fertility-restored F1 hybrids.
In theory, the cytoplasms of these four CMS lines are
derived from the respective Aegilops species (Ae.
kotschyi, Ae. variabilis, Ae. ventricosa and Ae.
bicornis). However, distinct differences were detected
between Aegilops and CMS lines. The variation of
mtDNA in Aegilops spp. and their respective CMS
lines may reflect the fertility divergence. Since a
variety of mtDNA mutations can cause the CMS trait,
it was not possible to determine which variation of
mtDNA patterns is linked with the CMS trait. Further
studies, are therefore needed to reveal the relationship
between the polymorphic markers and CMS trait.
In most cases, fertility restorer genes appear to
regulate gene expression at a transcriptional or
posttranscriptional level (Singh et al., 1996; Li et al.,
1998). Recent studies also have shown evidence of
fertility restoration through mtDNA alterations. In
maize, spontaneous reversion to fertility in CMS-S
maize involves alterations of the mitochonrial genome
(Schardl et al., 1985). In common bean, fertility
restorer gene Fr locus results in the loss of a particular
CMS-associated mtDNA region (He et al., 1995). Our
results demonstrated the variation of mtDNA in CMS
lines and their fertility-restored F1 hybrids. It's
possible that fertility restoration involves a strong
influence of the restorer genes on mtDNA
organization. Although the differences in RAPD
patterns are not necessarily associated with CMS trait,
they can be informative molecular markers to map
CMS-associated gene regions. Further studies are under
way converting the RAPD markers into SCAR markers
and cloning CMS-associated mitochondrial gene.
Acknowledgements
We thank Xudong Zhu for γ-ray irradiation and this work is supported by a
funding (2009ZX08009-112B) from the Ministry of Agriculture, China.
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