Abstract
We characterized two maize (Zea mays) mutants, zmsmu2-1 and zmsmu2-3, that result from insertion of a Mutator (Mu) transposable element in the first exon of a gene homologous to the nematode gene, smu-2, which is involved in RNA splicing. In addition to having a starchy endosperm with reduced levels of zein storage proteins, homozygous zmsmu2-1 mutants manifest a number of phenotypes, including defective meristem development. The zmsmu2 mutants have poor seedling viability and surviving plants are sterile. The gene encoding ZmSMU2 is expressed in the endosperm, embryo, and shoot apex, which explains the pleiotropic nature of the mutation. We found that proper expression of Zmsmu2 is required for efficient ribosomal RNA processing, ribosome biogenesis, and protein synthesis in developing endosperm. Based on the pleiotropic nature of the mutations and the known function of animal Zmsmu2 homologs, we propose a possible role for ZmSMU2 in the development of maize endosperm, as well as a mechanism by which misregulation of zmsmu2 causes the mutant phenotypes.
Highlights
We characterized two maize (Zea mays) mutants, zmsmu2-1 and zmsmu2-3, that result from insertion of a Mutator (Mu) transposable element in the first exon of a gene homologous to the nematode gene, smu-2, which is involved in RNA splicing
We found that zmsmu2-1 endosperm manifests defective ribosomal RNA processing and ribosome biogenesis, as well as inefficient protein synthesis on a global level
A subset of these mutants, mto38 through mto50, showed a similar pattern of reduced zein synthesis, and they were later found to have originated from the same F1 cross of a Mu-active and a Muinactive parental line
Summary
We characterized two maize (Zea mays) mutants, zmsmu and zmsmu, that result from insertion of a Mutator (Mu) transposable element in the first exon of a gene homologous to the nematode gene, smu-2, which is involved in RNA splicing. In addition to having a starchy endosperm with reduced levels of zein storage proteins, homozygous zmsmu mutants manifest a number of phenotypes, including defective meristem development. The gene encoding ZmSMU2 is expressed in the endosperm, embryo, and shoot apex, which explains the pleiotropic nature of the mutation. We found that proper expression of Zmsmu is required for efficient ribosomal RNA processing, ribosome biogenesis, and protein synthesis in developing endosperm. Based on the pleiotropic nature of the mutations and the known function of animal Zmsmu homologs, we propose a possible role for ZmSMU2 in the development of maize endosperm, as well as a mechanism by which misregulation of zmsmu causes the mutant phenotypes. Studies of the o2, fl, and De-B30 mutants make it clear that zein proteins influence endosperm texture, other opaque mutants suggest there must be additional factors that contribute to this phenotype. We found that zmsmu endosperm manifests defective ribosomal RNA (rRNA) processing and ribosome biogenesis, as well as inefficient protein synthesis on a global level
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