<i>MUN</i> (<i>MERISTEM UNSTRUCTURED</i>), encoding a SPC24 homolog of NDC80 kinetochore complex, affects development through cell division in <i>Arabidopsis thaliana</i>

  • Jinwoo Shin
    Laboratory of Plant Developmental Genetics School of Biological Sciences Plant Genomics and Breeding Institute Seoul National University Seoul 08826 Korea
  • Goowon Jeong
    Laboratory of Plant Developmental Genetics School of Biological Sciences Plant Genomics and Breeding Institute Seoul National University Seoul 08826 Korea
  • Jong‐Yoon Park
    Laboratory of Plant Developmental Genetics School of Biological Sciences Plant Genomics and Breeding Institute Seoul National University Seoul 08826 Korea
  • Hoyeun Kim
    Laboratory of Plant Developmental Genetics School of Biological Sciences Plant Genomics and Breeding Institute Seoul National University Seoul 08826 Korea
  • Ilha Lee
    Laboratory of Plant Developmental Genetics School of Biological Sciences Plant Genomics and Breeding Institute Seoul National University Seoul 08826 Korea

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<jats:title>Summary</jats:title><jats:p>Kinetochore, a protein super‐complex on the centromere of chromosomes, mediates chromosome segregation during cell division by providing attachment sites for spindle microtubules. The <jats:styled-content style="fixed-case">NDC</jats:styled-content>80 complex, composed of four proteins, <jats:styled-content style="fixed-case">NDC</jats:styled-content>80, <jats:styled-content style="fixed-case">NUF</jats:styled-content>2, <jats:styled-content style="fixed-case">SPC</jats:styled-content>24 and <jats:styled-content style="fixed-case">SPC</jats:styled-content>25, is localized at the outer kinetochore and connects spindle fibers to the kinetochore. Although it is conserved across species, functional studies of this complex are rare in Arabidopsis. Here, we characterize a recessive mutant, <jats:italic>meristem unstructured‐1</jats:italic> (<jats:italic>mun‐1</jats:italic>), exhibiting an abnormal phenotype with unstructured shoot apical meristem caused by ectopic expression of the <jats:italic><jats:styled-content style="fixed-case">WUSCHEL</jats:styled-content></jats:italic> gene in unexpected tissues. <jats:italic>mun‐1</jats:italic> is a weak allele because of the insertion of T‐<jats:styled-content style="fixed-case">DNA</jats:styled-content> in the promoter region of the <jats:italic><jats:styled-content style="fixed-case">SPC</jats:styled-content>24</jats:italic> homolog. The mutant exhibits stunted growth, embryo arrest, <jats:styled-content style="fixed-case">DNA</jats:styled-content> aneuploidy, and defects in chromosome segregation with a low cell division rate. Null mutants of <jats:italic><jats:styled-content style="fixed-case">MUN</jats:styled-content></jats:italic> from <jats:styled-content style="fixed-case">TALEN</jats:styled-content> and <jats:styled-content style="fixed-case">CRISPR</jats:styled-content>/Cas9‐mediated mutagenesis showed zygotic embryonic lethality similar to <jats:italic>nuf2‐1</jats:italic>; however, the null mutations were fully transmissible via pollen and ovules. Interactions among the components of the <jats:styled-content style="fixed-case">NDC</jats:styled-content>80 complex were confirmed in a yeast two‐hybrid assay and <jats:italic>in planta</jats:italic> co‐immunoprecipitation. <jats:styled-content style="fixed-case">MUN</jats:styled-content> is co‐localized at the centromere with <jats:styled-content style="fixed-case">HTR</jats:styled-content>12/<jats:styled-content style="fixed-case">CENH</jats:styled-content>3, which is a centromere‐specific histone variant, but <jats:styled-content style="fixed-case">MUN</jats:styled-content> is not required to recruit <jats:styled-content style="fixed-case">HTR</jats:styled-content>12/<jats:styled-content style="fixed-case">CENH</jats:styled-content>3 to the kinetochore. Our results support that <jats:styled-content style="fixed-case">MUN</jats:styled-content> is a functional homolog of <jats:styled-content style="fixed-case">SPC</jats:styled-content>24 in Arabidopsis, which is required for proper cell division. In addition, we report the ectopic generations of stem cell niches by the malfunction of kinetochore components.</jats:p>

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