Supplementary material
Table S1. Primers used in this study.
Name / Primera / 5′-CTTAGCCAAACTTCATTGTTATCTG-3′
b / 5′-AATCCAGATCCCCCGAATTA-3′
c / 5′-AGTCGGTGTTGATGCCTGTA-3′
osa-miR156e-F / 5′-CTTGGATCCCTGGCAACTGCGCCTATGCA-3′
osa-miR156e-R / 5′-CTTGGTACCTAAATCCACTGGCCGGTGG-3′
osa-miR156eA-F / 5′-CTTGGTACCGAGATCTAGAACCTGGCAACTGC-3′
osa-miR156eA-R / 5′-CTTGGATCCAGGCTAGCGCATGCTACCTT-3′
OsTB1S / 5′-CTTGTCGACGCGTTGCTGCTGCTACTGCT-3′
OsTB1A / 5′-CTTGAGCTCCCTTCGACGAGACGATGACG-3′
TEV-L / 5′-CTTGTCGACACTGGCAAGACTATCAGAATTC-3′
TER-R / 5′-GCCAAGCTTGCATGCCTGCAG-3′
TERR2 / 5′-CTTGAGCTCGCCAAGCTTGCATGCCTGCAG-3′
GUSF / 5′-ACGACTCGTCCGTCCTGTAGAA-3′
GUSR / 5′-CGGTTCGTTGGCAATACTCC-3′
U6-F / 5′-TACAGATAAGATTAGCATGGCCCC-3′
U6-R / 5′-GGACCATTTCTCGATTTGTACGTG-3′
MIR156e-St-RT / 5′-GTCGTATCCAGTGCAGGGTCCGAGGTATTCGCACTGGATACGACGTGCTC-3′
MIR156e-F / 5′-CGGCTGACAGAAGAGAGTGA-3′
MIRNA-R / 5′-GTGCAGGGTCCGAGGT-3′
D27S / 5′-TCTGGGCTAAAGAATGAAAAGGA-3′
D27A / 5'-AGAGCTTGGGTCACAATCTCG-3'
D14S / 5'-CATCCGACGACCTGACCTCT-3'
D14A / 5'-ATCTCCTCCAGCTCGAACCC-3'
HTD1S / 5'-ACCTCGTCCAGAAGCGTGAGT-3'
HTD1A / 5'-AGGCCCAGTCGTGGATCA-3'
D10S / 5'-CGGTGACCCTGCCATCAT-3'
D10A / 5'-CGTCCTTGCCCCTTAACAATC-3'
D3S / 5'-GGGATGGCGTGTGCAGAT-3'
D3A / 5'-TCAACATGCCCGATAATGACA-3'
TB1S / 5'-TCTCGCGTTTATCCGGAGTT-3'
TB1A / 5'-CATGCGATGACCAAACCAAA-3'
OsIPT4S / 5'-AGCTGAGCTAGCGATCAACAC-3'
OsIPT4A / 5'-TGTACGCCTGCATGGTGA-3'
OsIPT7S / 5'-GAAGACCAAGCTGTCCATCG-3'
OsIPT7A / 5'-GGCCGTCATAGAGCTGAATC-3'
MOC1S / 5'-ACCGTCGTTGTAGTAGCTCTGG-3'
MOC1A / 5'-CACCGCTGTTGTTATCCGTGT-3'
Ubiquitin5-F / 5'-AACCAGCTGAGGCCCAAGA-3'
Ubiquitin5-R / 5'-ACGATTGATTTAACCAGTCCATGA-3'
GAPDH-F / 5'-CGACCCGTTCATCACCACCGAC-3'
GAPDH-R / 5'-AGCTAGCAGCCCTTCCACCTCTCCA-3'
Figure S1Co-segregation between the phenotype and genotype in the T2 generationof H.
(a) The PCR genotyping ofHsegregants in T2 generation. Samples5, 9, 14, 18, 23, 26, 30, 33, and 35, which exhibited wild type phenotype(WT) amplified only the genomic DNA (a + c); samples 2, 6, 7, 13, 19, 20, 28, 31, 37, and 40, which showedMphenotype amplified only the sequence (b + c) and were homozygous; the other samples amplified both bands and weretherefore heterozygous, and showedH phenotype; (b) phenotype segregation in the T2 generation ofH.
Figure S2 Phenotype segregation in the T1 generations of miR156e-OX (a) and miR156eA-OX (b).
Figure S3 Schematic diagrams of the GAL4–UAS transactivation system.
pEGFP: activator vector; pGOC17-156e: effector vector; GAL4-VP16: a fusion gene of yeast transcriptional activator GAL4 DNA-binding domain with the Herpes simplex virus VP16 activation domain; EGFP: GFP with enhanced activity; GUSplus: a modifiedβ-glucuronidase; 6XUAS: upstream activator sequence with six repeats; Hph: hygromycin phosphotransferase; MP: minimal promoter; MCS: multiple cloning sites; LB, left border; RB, right border of the T-DNA.