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A semi‐dominant mutation in the ribosomal protein L10 gene suppresses the dwarf phenotype of the acl5 mutant in Arabidopsis thaliana
Author(s) -
Imai Akihiro,
Komura Mio,
Kawano Eri,
Kuwashiro Yoshitaka,
Takahashi Taku
Publication year - 2008
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2008.03647.x
Subject(s) - biology , genetics , mutant , gene , open reading frame , ribosomal protein , phenotype , start codon , arabidopsis , arabidopsis thaliana , microbiology and biotechnology , ribosome , messenger rna , rna , peptide sequence
Summary Disruption of the Arabidopsis thaliana ACAULIS5 ( ACL5 ) gene, which has recently been shown to encode thermospermine synthase, results in a severe dwarf phenotype. A previous study showed that sac51‐d , a dominant suppressor mutant of acl5‐1 , has a premature termination codon in an upstream open reading frame (ORF) of SAC51 , which encodes a putative transcription factor, and suggested the involvement of upstream ORF‐mediated translational control in ACL5 ‐dependent stem elongation. Here we report the identification of a gene responsible for sac52‐d , another semi‐dominant suppressor mutant of acl5‐1 . SAC52 encodes ribosomal protein L10 (RPL10A), which is highly conserved among eukaryotes and implicated in translational regulation. Transformation of acl5‐1 mutants with a genomic fragment containing the sac52‐d allele rescued the dwarf phenotype of acl5‐1 . GUS reporter activity under the control of a SAC51 promoter with its upstream ORF was higher in acl5‐1 sac52‐d than in acl5‐1 , suggesting that suppression of the acl5‐1 phenotype by sac52‐d is attributable, in part, to enhanced translation of certain transcripts including SAC51 . We also found that a T‐DNA insertion allele of SAC52/RPL10A causes lethality in the female gametophyte.