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Title: Morphological and Cytological Study in a New Type of Cytoplasmic Male Sterile Line CMS-GIG2 in Sunflower (Helianthus annuus)

Authors
item Zhang, Jichong -
item Wang, Lijuan -
item Zhao, Aiguo -
item Liu, Hui -
item Jan, Chao-Chien
item Qi, Dongmei -
item Liu, Gongshe -

Submitted to: Plant Breeding
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: March 19, 2009
Publication Date: April 1, 2009
Citation: Zhang, J., Wang, L., Zhao, A., Liu, H., Jan, C.C., Qi, D., Liu, G. 2009. Morphological and Cytological Study in a New Type of Cytoplasmic Male Sterile Line CMS-GIG2 in Sunflower (Helianthus annuus). Plant Breeding. 129:19-23.

Interpretive Summary: Cytoplasmic male sterility (CMS) is a maternally inherited trait that has been described in more than 150 plant species, and is characterized by the inability to produce functional pollen grains, but both vegetative and female development is unaffected. Hybrid sunflower production is currently depended totally on a single CMS-PET1 cytoplasm and one fertility restoration gene Rf1. The objectives of this study were to compare a new CMS-GIG2-lemon with CMS-PET1 on male gamete development and cytoplasmic specific genes, and their reaction to restoration tester lines. Our results indicated that CMS-GIG2-lemon was different from CMS-PET1 and other CMS sources reported. The fertility restoration gene identified is a major dominant gene capable of restoring fertility fully in heterozygous condition. This new CMS and fertility restoration combination will broaden the genetic basis of cultivated sunflower and to reduce the potential risk of vulnerability.

Technical Abstract: A new cytoplasmic male sterility (CMS) in sunflower anthers, termed lemon CMS-GIG2, has been further confirmed by crossing with the maintenance line and restoration line of CMS-PET1, both of which maintain the male sterility of CMS-GIG2. Light microscopy observation of anther sections showed that both the middle layer and tapetal cells expand radially rather than degrade over time, followed by failure to form tetrads and normal microspores. This morphological defect leading to male sterility in CMS-GIG2 differs from that observed in the PET1 CMS type. PCR amplification with the mitochondrial-specific primers for atp6 showed an apparent variation between CMS-PET1 and CMS-GIG2. Comparison of the nucleotide sequence of the atp6 gene also showed a difference between CMS-PET1 and CMS-GIG2. Nuclear meiotic division in CMS-GIG2 was observed with DAPI staining, indicating that microspore formation was disrupted before the meiotic cytokinesis was completed.

   
 
 
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