ArticleTAG. Theoretical and applied genetics. Theoretische und angewandte Genetik2011
High-resolution genetic mapping and candidate gene identification of the SLP1 locus that controls glume development in rice.
Article in TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 15 citations in OpenAlex.
- Molecular characterization of SPL gene family during flower morphogenesis and regulation in blueberry.BMC plant biology · 2023Article
- Characterization of a new rice OsMADS1 null mutant generated by homologous recombination-mediated gene targeting.Planta · 2021Article
- Evidence That the Origin of Naked Kernels During Maize Domestication Was Caused by a Single Amino Acid Substitution in tga1.Genetics · 2015Article
- Down-regulation of a LBD-like gene, OsIG1, leads to occurrence of unusual double ovules and developmental abnormalities of various floral organs and megagametophyte in rice.Journal of experimental botany · 2015Article
- Differential Proteomic Analysis Using iTRAQ Reveals Alterations in Hull Development in Rice (Oryza sativa L.).PloS one · 2015Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stunted lemma palea 1 (slp1) is a rice mutant that displays dwarfism, shortened inflorescence lengths, severely degenerated lemmas/paleas, and sterility. The SLP1 locus was mapped between markers RM447 and D275 in the distal region of the long arm of chromosome 8, using the F2 progeny derived from the cross between the Slp1/slp1 mutant (Oryza sativa subsp. japonica) and the variety Taichung Native 1 (TN1, O. sativa subsp. indica). The SLP1 locus was further delimited to a 46.4-kb genomic region containing three putative genes: OsSPL16, OsMADS45, and OsMADS37. Comparisons of the sequence variations and expression levels of the three candidate genes between wild-type plants and homozygous slp1 mutants suggested that a missense mutation in the sixth amino acid of the OsSPL16 protein was likely responsible for the slp1 mutant phenotypes.
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