bims-plasge Biomed News
on Plastid genes
Issue of 2019‒09‒15
three papers selected by
Vera S. Bogdanova
Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences

  1. Theor Appl Genet. 2019 Sep 07.
      KEY MESSAGE: Two stem rust resistance genes identified on chromosome arms 2BL and 6AL of the cultivated emmer wheat accession PI 193883 can be used for protecting modern varieties against Ug99 strains. The wheat research community consistently strives to identify new genes that confer resistance to stem rust caused by the fungal pathogen Puccinia graminis f. sp. tritici Eriks & E. Henn (Pgt). In the current study, our objective was to identify and genetically characterize the stem rust resistance derived from the cultivated emmer accession PI 193883. A recombinant inbred line population developed from a cross between the susceptible durum wheat line Rusty and PI 193883 was genotyped and evaluated for reaction to Pgt races TTKSK, TRTTF, and TMLKC. Two QTLs conferring resistance were identified on chromosome arms 2BL (QSr.fcu-2B) and 6AL (QSr.fcu-6A). The stem rust resistance gene (Sr883-2B) underlying QSr.fcu-2B was recessive, and based on its physical location it is located proximal to the Sr9 region. QSr.fcu-6A was located in the Sr13 region, but PI 193883 is known to carry the susceptible haplotype S4 for Sr13, indicating that the gene underlying QSr.fcu-6A (Sr883-6A) is likely a new allele of Sr13 or a gene residing close to Sr13. Three IWGSC scaffold-based simple sequence repeat (SSR) and two SNP-based semi-thermal asymmetric reverse PCR (STARP) markers were developed for the Sr883-2B region, and one STARP marker was developed for Sr883-6A. Sr883-2B was epistatic to Sr883-6A for reaction to TTKSK and TRTTF, and the two genes had additive effects for TMLKC. These two genes and the markers developed in this research provide additional resources and tools for the improvement in stem rust resistance in durum and common wheat breeding programs.
  2. Plant Physiol. 2019 Sep 13. pii: pp.00922.2019. [Epub ahead of print]
      In chloroplasts and plant mitochondria, specific cytidines in mRNAs are post-transcriptionally converted to uridines by RNA editing. Editing sites are recognized by nucleus-encoded RNA-binding proteins of the pentatricopeptide repeat (PPR) family, which bind upstream of the editing site in a sequence-specific manner and direct the editing activity to the target position. Editing sites have been lost many times during evolution by C-to-T mutations. Loss of an editing site is thought to be accompanied by loss or degeneration of its cognate PPR protein. Consequently, foreign editing sites are usually not recognized when introduced into species lacking the site. Previously, the spinach (Spinacia oleracea) psbF-26 editing site was introduced into the tobacco (Nicotiana tabacum) plastid genome. Tobacco lacks the psbF-26 site and cannot edit it. Expression of the "unedited" PsbF protein resulted in impaired photosystem II function. In Arabidopsis (Arabidopsis thaliana), the PPR protein LPA66 is required for editing at psbF-26. Here, we show that introduction of the Arabidopsis LPA66 reconstitutes editing of the spinach psbF-26 site in tobacco and restores a wild-type-like phenotype. Our findings define the minimum requirements for establishing novel RNA editing sites and suggest that the evolutionary dynamics of editing patterns is largely explained by co-evolution of editing sites and PPR proteins.
  3. Chromosoma. 2019 Sep 07.
      The Ph1 gene is the principal regulator of homoeologous chromosome pairing control (HECP) that ensures the diploid-like meiotic chromosome pairing behavior of polyploid wheat. The HECP control was speculated to have evolved after the first event of polyploidization. With the objective to accurately understand the evolution of the HECP control, wild emmer wheat accessions previously known to differ for HECP control were characterized for the structure and expression of the candidate Ph1 gene, C-Ph1. The C-TdPh1-5A and 5B gene copies of emmer wheat showed 98 and 99% DNA sequence similarity respectively with the corresponding hexaploid wheat copies. Further, the C-TdPh1-5B carried the C-Ph1-5B specific structural changes and transcribed three splice variants as observed in the hexaploid wheat. Further, single nucleotide changes differentiating accessions varying for HECP control were identified. Analyzed by quantitative expression analysis, the wild emmer accessions with HECP control showed ~ 10,000-fold higher transcript abundance of the C-TdPh1-5B copy during prophase-I compared to accessions lacking the control. Differential transcriptional regulation of C-TdPh1-5B splice variants further revealed that C-Ph1-5Balt1 variant is mainly responsible for differential accumulation of C-Ph1-5B copy in accessions with HECP control. Taken together, these results showed that the HECP control evolved via transcriptional regulation of splice variants during meiosis.
    Keywords:  Gene expression; Homoeologous chromosome pairing control; Meiosis; Ph1 gene