Rearrangements in maize mitochondrial genes

Genome ◽  
1989 ◽  
Vol 31 (1) ◽  
pp. 160-168 ◽  
Author(s):  
Lino L. Fragoso ◽  
Scott E. Nichols ◽  
Charles S. Levings III

Recombination is a significant cause of maize mitochondrial gene mutations. Chimeric genes are often found in the mitochondria of cytoplasmic male-sterile maize. They are created by rearrangements involving intramolecular and intermolecular recombination. Herein we describe the effect of rearrangements on the chromosomal location, flanking and coding regions of several maize mitochondrial genes.Key words: recombination, organelle, chimeric genes.

A few extra genes that are not found in the mitochondria of other organisms are encoded by plant mitochondrial genomes. Current evidence suggests that the cytoplasmic male sterility (CMS) trait of maize is due to mitochondrial gene mutations. In the sterile maize (CMS-T) a unique mitochondrial gene, designated urf /13-T, appears to cause CMS and susceptibility to the fungal pathogen Helminthosporium maydis race T, and its pathotoxin, T-toxin. The urf 13-T gene encodes a 13 kDa polypeptide that is located in the mitochondrial membrane. In CMS-T two nuclear restorer genes, Rf 1 and Rf 2, countermand the CMS trait and restore viable pollen production. The Rf 1 locus appears to contribute to pollen restoration by reducing the expression of the 13 kDa protein. The function of the Rf 2 gene is unknown. T-toxin and the insecticide methomyl inhibit respiration of mitochondria from CMS-T but not from other maize cytoplasms. When the urf 13-T gene is transformed into E. coli cells and expressed, bacterial respiration is inhibited by both T-toxin and methomyl. Respiration is not inhibited by these compounds in the absence of the 13 kDa protein or with a truncated version of the protein. These studies indicate that the 13 kDa protein is responsible for conferring sensitivity to T-toxin and methomyl. The male-sterile cytoplasm, CMS-C, contains mutations of the mitochondrial genes atp 9, atp 6 and cox II. These mutations have resulted from rearrangements involving portions of mitochondrial genes and chloroplast DNA. One of these gene mutations may be responsible for CMS; however, we currently have no evidence confirming this possibility. Nevertheless, it is clear that different factors cause male sterility in CMS-T and CMS-C because the urf 13-T gene is only found in CMS-T.


2011 ◽  
pp. 20-21
Author(s):  
T.P. Suprunova ◽  
A.N. Logunov ◽  
V.V. Logunova ◽  
A.F. Agafonov

Molecular markers were used for screening of the onion plants of VNIISSOK's breeding for cytoplasmic male sterility. Allelic variations of the mitochondrial genes orfА501 and cob were reveled among studied onion samples. Use of the PCR-markers for these genes allowed identifying the cytoplasmic types of 14 onion genotypes. Application of these molecular markers in breeding program could help to select genotypes wit certain type of cytoplasm and may be useful for high throughput identification of cytoplasmic male sterile factors in large onion breeding populations.


2018 ◽  
Vol 95 (4) ◽  
pp. 715-726 ◽  
Author(s):  
Hongwei Xie ◽  
Xiaojue Peng ◽  
Mingjuan Qian ◽  
Yicong Cai ◽  
Xia Ding ◽  
...  

2021 ◽  
Author(s):  
Shiho Omukai ◽  
Shin-ich Arimura ◽  
Kinya Toriyama ◽  
Tomohiko Kazama

AbstractPlant mitochondrial genomes sometimes carry cytoplasmic male sterility (CMS)-associated genes. These genes have been harnessed in agriculture to produce high-yielding F1 hybrid seeds in various crops. The gene orf352 was reported to be an RT102-type CMS gene in rice (Oryza sativa), although a causal demonstration of its role in CMS is lacking. Here, we employed mitochondrion-targeted transcription activator-like effector nucleases (mitoTALENs), to knock out orf352 from the mitochondrial genome in the cytoplasmic male sterile rice RT102A. We isolated 18 independent transformation events in RT102A that resulted in genome editing of orf352, including its complete removal from the mitochondrial genome in several plants. Sequence analysis around the mitoTALEN target sites revealed the repair of their induced double-strand breaks via homologous recombination. Near the 5ʹ target site, repair involved sequences identical to orf284, while repair of the 3ʹ target site yielded various new sequences that generated new chimeric genes consisting orf352 fragments. Plants with a new mitochondrial gene encoding amino acids 179 to 352 of ORF352 exhibited the same shrunken pollen grain phenotype as RT102A, whereas plants either lacking orf352 or harboring a new gene encoding amino acids 211 to 352 of ORF352 showed partial rescue of pollen viability and germination, although they failed to set seed. These results demonstrated that disruption of orf352 partially restored pollen development, indicating that amino acids 179 to 210 from ORF352 may contribute to the establishment of pollen abortion.


2009 ◽  
Vol 35 (9) ◽  
pp. 1620-1627 ◽  
Author(s):  
Long-Yu ZHANG ◽  
Hong-Xia LI ◽  
Gai-Sheng ZHANG ◽  
Jun-Sheng WANG ◽  
Yan-Fen HAN ◽  
...  

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