Regulation of FLC nuclear import by coordinated action of the NUP62-subcomplex and importinβSAD2

Flowering locus C(FLC)is a central transcriptional repressor that controls flowering time.However,how FLC is imported into the nucleus is unknown.Here,we report that Arabidopsis nucleoporins 62(NUP62),NUP58,and NUP54 composed NUP62-subcomplex modulates FLC nuclear import during floral transition in an importinα-independent manner,via direct interaction.NUP62 recruits FLC to the cytoplasmic filaments and imports it into the nucleus through the NUP62-subcomplex composed central channel.Importinβsupersensitive to ABA and drought 2(SAD2),a carrier protein,is critical for FLC nuclear import and flower transition,which facilitates FLC import into the nucleus mainly through the NUP62-subcomplex.Proteomics,RNAseq,and cell biological analyses indicate that the NUP62-subcomplex mainly mediates the nuclear import of cargos with unconventional nuclear localization sequences(NLSs),such as FLC.Our findings illustrate the mechanisms of the NUP62-subcomplex and SAD2 on FLC nuclear import process and floral transition,and provide insights into the role of NUP62-subcomplex and SAD2 in protein nucleocytoplasmic transport in plants.

IQ67 DOMAIN protein 21 is critical for indentation formation in pavement cell morphogenesis

In plants, cortical microtubules anchor to the plasma membrane in arrays and play important roles in cell shape. However, the molecular mechanism of microtubule binding proteins, which connect the plasma membrane and cortical microtubules in cell morphology remains largely unknown. Here, we report that a plasma membrane and microtubule duallocalized IQ67 domain protein, IQD21, is critical for cotyledon pavement cell(PC) morphogenesis in Arabidopsis. iqd21 mutation caused increased indentation width, decreased lobe length, and similar lobe number of PCs, whereas IQD21 overexpression had a different effect on cotyledon PC shape. Weak overexpression led to increased lobe number, decreased indentation width, and similar lobe length, while moderate or great overexpression resulted in decreased lobe number, indentation width, and lobe length of PCs. Live-cell observations revealed that IQD21 accumulation at indentation regions correlates with lobe initiation and outgrowth during PC development. Cell biological and genetic approaches revealed that IQD21 promotes transfacial microtubules anchoring to the plasma membrane via its polybasic sites and bundling at the indentation regions in both periclinal and anticlinal walls. IQD21 controls cortical microtubule organization mainly through promoting Katanin 1-mediated microtubule severing during PC interdigitation. These findings provide the genetic evidence that transfacial microtubule arrays play a determinant role in lobe formation, and the insight into the molecular mechanism of IQD21 in transfacial microtubule organization at indentations and puzzle-shaped PC development.