Fine mapping<i>PsPS1</i>, a gene controlling pod softness that defines market type in pea (<i>Pisum sativum</i>)

Zhang, Peipei; Wang, Yonggang; Sun, Ting; Wu, Xinyang; Xia, Wenjun; Fang, Pingping; Pandey, Arun K.; Xu, Pei

doi:10.1111/pbr.13020

Cited by 4 publications

(6 citation statements)

References 53 publications

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“…Subsequent fine-mapping led to the delineation of a 1.33Mb interval (Chr4 18.18-19.51Mb, ZW6) (Extended Data Fig. 8a-e, and Supplementary [25][26]. We found that all the accessions with fasciated phenotypes were clustered together within haplotype 5 of this 1.33Mb interval (Extended Data Fig.…”

Section: Fasciationmentioning

confidence: 75%

“…24 and Supplementary Table 32) and differential gene expression analysis, we identified Psat02G0011300 as a gene candidate for PsOs1 (Supplementary Figs. [25][26], which encodes a SIAMESE-related protein (SIM/SMR), a cyclin-dependent protein kinase inhibitor (CKI), influencing cell division and enlargement during the cell cycle and consequently altering plant cell size 75 . Functional validation from the VIGS (Supplementary Fig.…”

Section: A Quantitative Trait Essential In Pea Breedingmentioning

confidence: 99%

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Genomic and Genetic Insights into Mendel’s Pea Genes

Feng,

Chen,

Hofer

et al. 2024

Preprint

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Pea,Pisum sativum, is an excellent model system through which Gregor Mendel established the foundational principles of inheritance. Surprisingly, till today, the molecular nature of the genetic differences underlying the seven pairs of contrasting traits that Mendel studied in detail remains partially understood. Here, we present a genomic and phenotypic variation map, coupled with haplotype-phenotype association analyses across a wide range of traits in a globalPisumdiversity panel. We focus on a genomics-enabled genetic dissection of each of the seven traits Mendel studied, revealing many previously undescribed alleles for the four characterized genes,R,Le,IandA, and elucidating the gene identities and mutations for the remaining three uncharacterized traits. Notably, we identify: (1) a ca. 100kb deletion upstream of theChlorophyll synthase(ChlG) gene, which generates aberrant transcripts and confers the yellow pod phenotype ofgpmutants; (2) an in-frame premature stop codon mutation in a Dodeca-CLE41/44 signalling peptide which explains the parchmentless mutant phenotype corresponding top; and (3) a 5bp in-frame deletion in aCIK-likereceptor kinase gene corresponding to the fasciated stem phenotypefa, which Mendel described in terms of flower position, and we postulate the existence of aModifier of fa(Mfa) locus that masks this meristem defect. Mendel noted the pleiotropy of theamutation, including inhibition of axil ring anthocyanin pigmentation, a trait we found to be controlled by allelic variants of the geneDwithin anR2R3-MYBgene cluster. Furthermore, we characterize and validate natural variation of a quantitative genetic locus governing both pod width and seed weight, characters that Mendel deemed were not sufficiently demarcated for his analyses. This study establishes a cornerstone for fundamental research, education in biology and genetics, and pea breeding practices.

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Section: Fasciationmentioning

confidence: 75%

Section: A Quantitative Trait Essential In Pea Breedingmentioning

confidence: 99%

Genomic and Genetic Insights into Mendel’s Pea Genes

Feng,

Chen,

Hofer

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

“…Subsequent fine-mapping led to the delineation of a 1.33Mb interval (Chr4 18.18-19.51Mb, ZW6) (Extended Data Fig. 8a-e, and Supplementary Table [17][18][19][25][26]. We found that all the accessions with fasciated phenotypes were clustered together within haplotype 5 of this 1.33Mb interval (Extended Data Fig.…”

Section: Fasciationmentioning

confidence: 78%

“…and differential gene expression analysis, we identified Psat02G0011300 as a gene candidate for PsOs1 (Supplementary Figs. [25][26], which encodes a SIAMESE-related protein (SIM/SMR), a cyclin-dependent protein kinase inhibitor (CKI), influencing cell division and enlargement during the cell cycle and consequently altering plant cell size 75 . Functional validation from the VIGS (Supplementary Fig.…”

Section: A Quantitative Trait Essential In Pea Breedingmentioning

confidence: 99%

Genomic and Genetic Insights into Mendel’s Pea Genes

Cheng,

Feng,

Chen

et al. 2024

Preprint

View full text Add to dashboard Cite

Pea, Pisum sativum, is an excellent model system through which Gregor Mendel established the foundational principles of inheritance. Surprisingly, till today, the molecular nature of the genetic differences underlying the seven pairs of contrasting traits that Mendel studied in detail remains partially understood. Here, we present a genomic and phenotypic variation map, coupled with haplotype-phenotype association analyses across a wide range of traits in a global Pisum diversity panel. We focus on a genomics-enabled genetic dissection of each of the seven traits Mendel studied, revealing many previously undescribed alleles for the four characterized genes, R, Le, I and A, and elucidating the gene identities and mutations for the remaining three uncharacterized traits. Notably, we identify: (1) a ca. 100kb deletion upstream of the Chlorophyll synthase (ChlG) gene, which generates aberrant transcripts and confers the yellow pod phenotype of gp mutants; (2) an in-frame premature stop codon mutation in a Dodeca-CLE41/44 signalling peptide which explains the parchmentless mutant phenotype corresponding to p; and (3) a 5bp in-frame deletion in a CIK-like receptor kinase gene corresponding to the fasciated stem phenotype fa, which Mendel described in terms of flower position, and we postulate the existence of a Modifier of fa (Mfa) locus that masks this meristem defect. Mendel noted the pleiotropy of the a mutation, including inhibition of axil ring anthocyanin pigmentation, a trait we found to be controlled by allelic variants of the gene D within an R2R3-MYB gene cluster. Furthermore, we characterize and validate natural variation of a quantitative genetic locus governing both pod width and seed weight, characters that Mendel deemed were not sufficiently demarcated for his analyses. This study establishes a cornerstone for fundamental research, education in biology and genetics, and pea breeding practices.

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“…The peas have a notably low reproductive coe cient, as compared to the food crops, such as wheat and rice (Li et For BSA-seq, it is not necessary for large segregating populations to map target genes, and it has been successfully employed in peas to identify candidate regions and develop linked molecular markers for various traits, including leaf shape (Zheng et al 2018), pod softness (Zhang et al 2022b), and disease resistance (Fondevilla et al 2022;Wu et al 2022). In this study, a 10.4 Mb candidate region in chr6LG2 associated with the FwS1 was pinpointed using the BSA-seq method.…”

Section: Discussionmentioning

confidence: 99%

Fine Mapping and Identification of a Fusarium Wilt Resistance Gene FwS1 in Pea

Deng,

Sun,

et al. 2024

Preprint

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Pea Fusarium wilt, incited by Fusarium oxysporum f. sp. pisi (Fop), has always been a devastating disease that causes severe yield losses and economic damage in pea-growing regions worldwide. The utilization of pea cultivars carrying resistance gene is the most efficient approach for managing this disease. In order to finely map resistance gene, a F2 population was established through the cross between Shijiadacaiwan 1 (resistant) and Y4 (susceptible). The resistance genetic analysis indicated that the Fop resistance in Shijiadacaiwan 1 was governed by a single dominant gene, named as FwS1. Based on the bulked segregant analysis sequencing (BSA-seq) analyses, the gene FwS1 was initially detected on chromosome 6 (i.e., linking group Ⅱ, chr6LG2), and subsequent linkage mapping with 589 F2 individuals fine-mapped the gene FwS1 into a 91.4 kb region. The further functional annotation and haplotype analysis confirmed that the gene Psat6g003960, characterized by a NB-ARC (nucleotide-binding adaptor shared by APAF-1, R proteins, and CED-4) domain, was considered as the most promising candidate gene. The encoding amino acids were altered by a “T/C” single-nucleotide polymorphism (SNP) in the first exon of the Psat6g003960, resulting in the observed differences of Fop resistance in peas. Based on this SNP locus, the molecular marker A016180 was determined to be a diagnostic marker for FwS1 by validating its specificity in both pea accessions and genetic populations with different genetic backgrounds. The FwS1 with diagnostic KASP marker A016180 could facilitate marker-assisted selection in resistance pea breeding in pea. In addition, upon comparing the candidate gene Psat6g003960 of 74SN3B and SJ1, it was noted that their sequences are identical, suggesting that the FwS1 and Fwf may be the same resistance gene against Fusarium wilt.

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Fine mappingPsPS1, a gene controlling pod softness that defines market type in pea (Pisum sativum)

Cited by 4 publications

References 53 publications

Genomic and Genetic Insights into Mendel’s Pea Genes

Genomic and Genetic Insights into Mendel’s Pea Genes

Genomic and Genetic Insights into Mendel’s Pea Genes

Fine Mapping and Identification of a Fusarium Wilt Resistance Gene FwS1 in Pea

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