Biomedical subjects

Christine D Chase

Publications and source records attributed to Christine D Chase.

5 recordsLinked to original sources

PubMed2006

Cytoplasmic male sterility: a window to the world of plant mitochondrial-nuclear interactions.

Mitochondrial function depends on the coordinate action of nuclear and mitochondrial genomes. The genetic dissection of these interactions presents special challenges in obligate aerobes, because the viability of these organisms depends on mitochondrial respiration. The plant trait cytoplasmic male sterility (CMS) is determined by the mitochondrial genome and is associated with a pollen sterility phenotype that can be suppressed or counteracted by nuclear genes known as restorer-of-fertility genes. Here, I review the nature and the origin of the genes that determine CMS, together with recent investigations that have exploited CMS to provide new insights into plant mitochondrial-nuclear communication. These studies have implicated mitochondrial signaling pathways, including those involved in regulating cell death and nuclear gene expression, in the elaboration of CMS. The molecular cloning of nuclear genes that restore fertility (i.e. restorer-of-fertility genes) has identified genes encoding pentatricopeptide-repeat proteins as key regulators of plant mitochondrial gene expression.

Cell Nucleus↗

PubMed2005

Genetically engineered cytoplasmic male sterility.

Cytoplasmic male sterility, conditioned by some maternally inherited plant mitochondrial genomes, is the most expedient method to produce uniform populations of pollen-sterile plants on a commercial scale. Plant mitochondrial genomes are not currently amenable to genetic transformation, but genetic manipulation of the plastid genome allows engineering of maternally inherited traits in some species. A recent study has shown that the Acinetobacter beta-ketothiolase gene, expressed in the Nicotiana tabacum plastid, conditions maternally inherited male sterility, laying the groundwork for new approaches to control pollen fertility in crop plants.

Cytoplasm↗

PubMed2004

Molecular-genetic characterization of CMS-S restorer-of-fertility alleles identified in Mexican maize and teosinte.

Restorer-of-fertility (Rf) alleles for S-type cytoplasmic male sterility (CMS-S) are prevalent in Mexican races of maize and teosinte. Forty-five Rf alleles from 26 races of maize and 6 Rf alleles from different accessions of teosinte were found to be homozygous viable, consistent with the hypothesis that they are naturally occurring Rf alleles. Mapping and allelism studies were performed to assess the number of genes represented by these 51 alleles. Forty-two of the Rf alleles mapped to the long arm of chromosome 2 (2L), and 5 of these were further mapped to the whp1-rf3 region. The Rf3 restoring allele, found in some U.S. maize inbred lines, cosegregates with internal processing of CMS-S mitochondrial transcripts. Three of the 5 mapped Rf alleles were associated with a similar RNA processing event. Allelism or tight linkage was confirmed between Rf3 and 2 teosinte alleles (Rf K-69-6 and Rf 9477) and between Rf3 and the Cónico Norteño allele Rf C-N (GTO 22). The rf3 region of 2L potentially encodes a complex of linked rf genes. The prevalence of restoring alleles in this chromosomal region, among normal-cytoplasm accessions of Mexican maize and teosinte, supports the conclusion that these alleles have functions in normal mitochondrial gene expression that by chance allow them to restore male fertility in S cytoplasm.

Chromosome Mapping↗

PubMed2003

A nuclear restorer-of-fertility mutation disrupts accumulation of mitochondrial ATP synthase subunit alpha in developing pollen of S male-sterile maize.

Mitochondrial biogenesis and function depend upon the interaction of mitochondrial and nuclear genomes. Forward genetic analysis of mitochondrial function presents a challenge in organisms that are obligated to respire. In the S-cytoplasmic male sterility (CMS-S) system of maize, expression of mitochondrial open reading frames (orf355-orf77) conditions collapse of developing haploid pollen. Nuclear restorer-of-fertility mutations that circumvent pollen collapse are often homozygous lethal. These spontaneous mutations potentially result from disruption of nuclear genes required for mitochondrial gene expression, in contrast to homozygous-viable restorer-of-fertility alleles that function to block or compensate for the expression of mitochondrial CMS genes. Consistent with this hypothesis, the homozygous-lethal restoring allele historically designated RfIII was shown to be recessive in diploid pollen produced by tetraploid CMS-S plants. Accordingly, the symbol for this allele has been changed to restorer-of-fertility lethal 1 (rfl1). In haploid rfl1 pollen, orf355-orf77 transcripts and mitochondrial transcripts encoding the alpha-subunit of the ATP synthase (ATPA) were decreased in abundance. Haploid rfl1 pollen failed to accumulate wild-type levels of ATPA protein, indicating that functional requirements for mitochondrial protein accumulation are relaxed in maize pollen. The CMS-S system and rfl mutations therefore allow for the selection of nuclear mutations disrupting mitochondrial biogenesis in a multicellular eukaryote.

Alleles↗

PubMed2002

Mitochondrial RNA editing truncates a chimeric open reading frame associated with S male-sterility in maize.

Adjacent mitochondrial open reading frames orf355 and orf77 are associated with S cytoplasmic male sterility (CMS-S) in maize, but the mechanisms leading to collapse of developing CMS-S pollen are unknown. Sequence similarity between orf77 and the mitochondrial ATP synthase subunit 9 (atp9) locus led us to examine RNA editing in orf77 and atp9 transcripts of pre-collapse CMS-S microspores. Editing of atp9 was not influenced by the presence of orf77 transcripts. Sequence analysis of cDNA clones demonstrated that atp9 transcripts are fully edited in CMS-S microspores. Orf77 nucleotides corresponding to edited nucleotides in atp9 were either not edited or edited inefficiently within the context of orf77, perhaps due to limited conservation of flanking sequences between orf77 and atp9. However, eight of ten orf77 cDNA clones carried an unexpected terminating edit that truncated orf77 to predict a peptide of 17 amino acids (ORF17) sharing significant identity with the C-terminal transmembrane domain of the ATP9 protein.

Amino Acid Sequence↗