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Article|01 Feb 2019|OPEN
SCR-22 of pollen-dominant S haplotype class is recessive to SCR-44 of pollen-recessive S haplotype class in Brassica rapa
Chun-Lei Wang1,2 , , Zhi-Ping Zhang1 , Eriko Oikawa2 and Hiroyasu Kitashiba2 , Takeshi Nishio,2 ,
1School of Horticulture and Plant Protection, Joint International Research Laboratory of Agriculture and Agri-Product Safety, Key Laboratory of Plant Functional Genomics of the Ministry of Education, Yangzhou University, 48 Wenhui East Road, Yangzhou 225009, People’s Republic of China
2Graduate School of Agricultural Science, Tohoku University, 468-1 Aza-Aoba, Aramaki, Aoba-ku, Sendai, Miyagi 980-0845, Japan
*Corresponding author. E-mail: wangcl@yzu.edu.cn,nishio@tohoku.ac.jp

Horticulture Research 6,
Article number: 25 (2019)
doi: https://doi.org/10.1038/s41438-018-0103-5
Views: 998

Received: 01 Jun 2018
Revised: 07 Oct 2018
Accepted: 14 Oct 2018
Published online: 01 Feb 2019

Abstract

SCR/SP11 encodes the male determinant of recognition specificity of self-incompatibility (SI) in Brassica species and is sporophytically expressed in the anther tapetum. Based on dominance relationships in pollen and nucleotide sequence similarity, the S haplotypes in Brassica have been classified as class I or class II, with class-I S haplotypes being dominant over class-II S haplotypes. Here, we revealed that S-22 in B. rapa belonging to class I is recessive to class-II S-44 and class-I S-36 in pollen, whereas it is dominant over S-60, S-40, and S-29 based on pollination tests. SCR/SP11 of S-22 (SCR-22) was sequenced, revealing that the deduced amino-acid sequence of SCR-22 has the longest C-terminal domain among the SCR/SP11 sequences. The expression of SCR-22 was found to be suppressed in S-22/S-44 and S-22/S-36 heterozygotes. Normal transcription of SCR-44 was considered to be due to the transcription suppression of Smi sRNA of the S-22 haplotype and a very low methylation state of the SCR-44 promoter region in the tapetum of S-22/S-44 heterozygotes. In SCR-22, only the cytosine residue located at the –37 bp position of the promoter region was hypermethylated in the tapetum of S-22/S-44 heterozygotes, and few methylated cytosines were detected in the promoter and coding regions of SCR-22 in S-22/S-36 heterozygotes. SCR-22 was also expressed in microspores in S-22 homozygotes but not in S-22/S-44 and S-22/S-36 heterozygotes. These results suggest that a mechanism different from class-II SCR/SP11 suppression may operate for the suppression of recessive class-I SCR-22 in S heterozygotes.