bims-plasge 2024-02-11 papers

Issue of 2024–02–11
two papers selected by
Vera S. Bogdanova, ИЦиГ СО РАН

Theor Appl Genet. 2024 Feb 09. 137(2): 47

Fine mapping of Ae-Ps4.5, a major locus for resistance to pathotype III of Aphanomyces euteiches in pea.

Clément Lavaud, Angélique Lesné, Théo Leprévost, Marie-Laure Pilet-Nayel.

KEY MESSAGE: QTL mapping and recombinant screening confirmed the major effect of QTL Ae-Ps4.5 on pea resistance to pathotype III of Aphanomyces euteiches and fine-mapped the QTL to a 3.06-Mb interval. Aphanomyces root rot, caused by Aphanomyces euteiches, is the most important disease of pea (Pisum sativum L.) worldwide. The development of pea-resistant varieties is a major challenge to control the disease. Previous linkage studies identified seven main resistance quantitative trait loci (QTL), including the QTL Ae-Ps4.5 associated with partial resistance in US nurseries infested by the pea pathotype III of A. euteiches. This study aimed to confirm the major effect of Ae-Ps4.5 on A. euteiches pathotype III, refine its interval, and identify candidate genes underlying the QTL. QTL mapping on an updated genetic map from the Puget × 90-2079 pea recombinant inbred line population identified Ae-Ps4.5 in a 0.8-cM confidence interval with a high effect (R2 = 89%) for resistance to the Ae109 reference strain of A. euteiches (pathotype III) under controlled conditions. However, the QTL mapping did not detect Ae-Ps4.5 for resistance to the RB84 reference strain of A. euteiches (pathotype I). Screening 224-pea BC5F2 plant progeny derived from three near-isogenic lines (NILs) carrying the 90-2079 allele at Ae-Ps4.5 in the Puget genetic background with 26 SNP markers identified 15 NILs showing recombination in the QTL interval. Phenotyping of the recombinant lines for resistance to the Ae109 strain of A. euteiches reduced the QTL to a physical interval of 3.06 Mb, containing 50 putative annotated genes on the Caméor pea genome V1a among which three candidate genes highlighted. This study provides closely linked SNP markers and putative candidate genes to accelerate pea breeding for resistant varieties to Aphanomyces root rot.

DOI: https://doi.org/10.1007/s00122-024-04548-6

Plant Commun. 2024 Feb 06. pii: S2590-3462(24)00056-7. [Epub ahead of print] 100836

Multiple factors interact in the editing of the PPR-E+ targeted sites in maize mitochondria and plastids.

Yong Wang, Zi-Qin Huang, Kai-Di Tian, Hao Li, Chunhui Xu, Bingyujie Xia, Bao-Cai Tan.

RNA C-to-U editing is essential for plant organellar gene expression. It is proposed that PPR-E+ proteins bind to target sites and recruit cytidine deaminase AtDYW2 facilitated by AtNUWA. We analyzed the function of ZmNUWA, ZmDYW2A, and ZmDYW2B and their relationship with other editing factors in maize. The zmdyw2a and zmdyw2b single mutants are normal, but the zmdyw2a::zmdyw2b and zmnuwa mutants are severely arrested in seed development. ZmNUWA, ZmDYW2A, and ZmDYW2B are dual-localized in mitochondria and plastids. Loss of ZmNUWA decreases the editing at 99 mitochondrial sites and 8 plastid sites. Surprisingly, loss of ZmDYW2A:ZmDYW2B affects almost the same set of sites targeted by PPR-E+ proteins. ZmNUWA interacts with ZmDYW2A and ZmDYW2B, suggesting that ZmNUWA recruits ZmDYW2A/2B in the editing of PPR-E+ protein targeted sites in maize. Further protein interaction analyses show that ZmNUWA and ZmDYW2A/2B interact with ZmMORF1, ZmMORF8, ZmMORF2, and ZmMORF9; and ZmOZ1 interacts with ZmORRM1, ZmDYW2A, ZmDYW2B, ZmMORF8, and ZmMORF9. These results suggest that the mitochondrial PPR-E+ editosome contains PPR-E+, ZmDYW2A/2B, ZmNUWA, and ZmMORF1/8, whereas the plastid PPR-E+ editosome composes of PPR-E+, ZmDYW2A/2B, ZmNUWA, ZmMORF2/8/9, ZmORRM1 and ZmOZ1 in maize.

Keywords: RNA editing; ZmDYW2A/2B; ZmNUWA; maize; plant organelles

DOI: https://doi.org/10.1016/j.xplc.2024.100836