ArticleG3 (Bethesda, Md.)2021
Mutation of the nuclear pore complex component, aladin1, disrupts asymmetric cell division in Zea mays (maize).
Article in G3 (Bethesda, Md.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- KATANIN is required for the formation of complete preprophase bands and subsequent division positioning in two asymmetric divisions of the maize stomatal complex.Journal of cell science · 2026Article
- The role of phase separation for RNA and protein transport through the nuclear pore complex.Journal of experimental botany · 2026Review
- Nuclear positioning and cell division site specification in plants.Journal of experimental botany · 2025Review
- Targeted seed EMS mutagenesis reveals a basic helix-loop-helix transcription factor underlying male sterility in sorghum.Genetics · 2025Article
- Identification of novel loci associated with starch content in maize kernels by a genome-wide association study using an enlarged SNP panel.Molecular breeding : new strategies in plant improvement · 2023Article
- Review
- QTL mapping and BSA-seq map a major QTL for the node of the first fruiting branch in cotton.Frontiers in plant science · 2023Article
- Transcriptional responses to gibberellin in the maize tassel and control by DELLA domain proteins.The Plant journal : for cell and molecular biology · 2022Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nuclear pore complex (NPC) regulates the movement of macromolecules between the nucleus and cytoplasm. Dysfunction of many components of the NPC results in human genetic diseases, including triple A syndrome (AAAS) as a result of mutations in ALADIN. Here, we report a nonsense mutation in the maize ortholog, aladin1 (ali1-1), at the orthologous amino acid residue of an AAAS allele from humans, alters plant stature, tassel architecture, and asymmetric divisions of subsidiary mother cells (SMCs). Crosses with the stronger nonsense allele ali1-2 identified complex allele interactions for plant height and aberrant SMC division. RNA-seq analysis of the ali1-1 mutant identified compensatory transcript accumulation for other NPC components as well as gene expression consequences consistent with conservation of ALADIN1 functions between humans and maize. These findings demonstrate that ALADIN1 is necessary for normal plant development, shoot architecture, and asymmetric cell division in maize.
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