Genome-wide study on the polysomic genetic factors conferring plasticity of flower sexuality in hexaploid persimmon
Author(s) -
Kanae Masuda,
Eiji Yamamoto,
Kenta Shirasawa,
Noriyuki Onoue,
Atsushi Kono,
Koichiro Ushijima,
Yasutaka Kubo,
Ryutaro Tao,
Isabelle Henry,
Takashi Akagi
Publication year - 2020
Publication title -
dna research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 98
eISSN - 1756-1663
pISSN - 1340-2838
DOI - 10.1093/dnares/dsaa012
Subject(s) - biology , genetics , retrotransposon , diospyros kaki , genotype , gene , genome , population , allele , botany , transposable element , demography , sociology
Sexuality is one of the fundamental mechanisms that work towards maintaining genetic diversity within a species. In diploid persimmons (Diospyros spp.), separated sexuality, the presence of separate male and female individuals (dioecy), is controlled by the Y chromosome-encoded small-RNA gene, OGI. On the other hand, sexuality in hexaploid Oriental persimmon (Diospyros kaki) is more plastic, with OGI-bearing genetically male individuals, able to produce both male and female flowers (monoecy). This is thought to be linked to the partial inactivation of OGI by a retrotransposon insertion, resulting in DNA methylation of the OGI promoter region. To identify the genetic factors regulating branch sexual conversion, genome-wide correlation/association analyses were conducted using ddRAD-Seq data from an F1 segregating population, and using both quantitative and diploidized genotypes, respectively. We found that allelic ratio at the Y-chromosomal region, including OGI, was correlated with male conversion based on quantitative genotypes, suggesting that OGI can be activated in cis in a dosage-dependent manner. Genome-wide association analysis based on diploidized genotypes, normalized for the effect of OGI allele dosage, detected three fundamental loci associated with male conversion. These loci underlie candidate genes, which could potentially act epigenetically for the activation of OGI expression.
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