著者

Yoshimi Nakano Maki Kawai Moeca Arai Sumire Fujiwara

出版者

Japanese Society for Plant Biotechnology

雑誌

Plant Biotechnology (ISSN:13424580)

巻号頁・発行日

vol.40, no.4, pp.337-344, 2023-12-25 (Released:2023-12-25)

参考文献数

26

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Correct flower organ formation at the right timing is one of the most important strategies for plants to achieve reproductive success. Ectopic overexpression of LATE FLOWERING (LATE) is known to induce late flowering, partly through suppressing expression of the florigen-encoding gene FLOWERING LOCUS T (FT) in Arabidopsis. LATE is one of the C2H2 zinc finger transcription factors, and it has a canonical transcriptional repression domain called the ethylene-responsive element-binding factor-associated amphiphilic repression (EAR) motif at the end of its C terminus. Therefore, LATE is considered a transcriptional repressor, but its molecular function remains unclear. Our genome-edited late mutants exhibited no distinct phenotype, even in flowering, indicating the presence of redundancy from other factors. To reveal the molecular function of LATE and factors working with it, we investigated its transcriptional activity and interactions with other proteins. Transactivation activity assay showed that LATE possesses transcriptional repression ability, which appears to be attributable to both the EAR motif and other sequences. Yeast two-hybrid assay showed the EAR motif-mediated interaction of LATE with TOPLESS, a transcriptional corepressor. Moreover, LATE could also interact with CRABS CLAW (CRC), one of the most important regulators of floral meristem determinacy, through sequences in LATE other than the EAR motif. Our findings demonstrated the possibility that LATE can form a transcriptional repression complex with CRC for floral meristem determinacy.

著者

Aili Ailizati Isura Sumeda Priyadarshana Nagahage Atsuko Miyagi Toshiki Ishikawa Maki Kawai-Yamada Taku Demura Masatoshi Yamaguchi

出版者

Japanese Society for Plant Biotechnology

雑誌

Plant Biotechnology (ISSN:13424580)

巻号頁・発行日

vol.39, no.2, pp.147-153, 2022-06-25 (Released:2022-06-25)

参考文献数

29

被引用文献数

1

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An Arabidopsis NAC domain transcription factor VND-INTERACTING2 (VNI2) was originally isolated as an interacting protein with another NAC domain transcription factor, VASCULAR-RELATED NAC-DOMAIN7 (VND7), a master regulator of xylem vessel element differentiation. VNI2 inhibits transcriptional activation activity of VND7 by forming a protein complex. Here, to obtain insights into how VNI2 regulates VND7, we tried to identify the amino acid region of VNI2 required for inhibition of VND7. VNI2 has an amino acid sequence similar to the ETHYLENE-RESPONSIVE ELEMENT BINDING FACTOR (ERF)-associated amphiphilic repression (EAR) motif, conserved in transcriptional repressors, at the C-terminus. A transient expression assay showed that the EAR-like motif of VNI2 was not required for inhibition of VND7. The C-terminal deletion series of VNI2 revealed that 10 amino acid residues, highly conserved in the VNI2 orthologs contributed to effective repression of the transcriptional activation activity of VND7. Observation of transgenic plants ectopically expressing VNI2 showed that the identified 10 amino acid sequence strongly affected xylem vessel formation and plant growth. These data indicated that the 10 amino acid sequence of VNI2 has an important role in its transcriptional repression activity and negative regulation of xylem vessel formation.

著者

Aili Ailizati Isura Sumeda Priyadarshana Nagahage Atsuko Miyagi Toshiki Ishikawa Maki Kawai-Yamada Taku Demura Masatoshi Yamaguchi

出版者

Japanese Society for Plant Biotechnology

雑誌

Plant Biotechnology (ISSN:13424580)

巻号頁・発行日

vol.38, no.4, pp.415-420, 2021-12-25 (Released:2021-12-25)

参考文献数

29

被引用文献数

4

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A NAC domain transcription factor, VND-INTERACTING2 (VNI2) is originally isolated as an interacting protein with another NAC domain transcription factor, VASCULAR-RELATED NAC-DOMAIN7 (VND7), a master regulator of xylem vessel element differentiation. VND7 directly or indirectly induces expression of a number of genes associated with xylem vessel element differentiation, while VNI2 inhibits the transcriptional activation activities of VND7 by forming a protein complex. VNI2 is expressed at an earlier stage of xylem vessel element differentiation than VND7. Here, to investigate whether VND7 also affects VNI2, a transient expression assay was performed. We demonstrated that VND7 downregulated VNI2 expression. Other transcription factors involved in xylem vessel formation did not show the negative regulation of VNI2 expression. Rather, MYB83, a downstream target of VND7, upregulated VNI2 expression. By using the deletion series of the VNI2 promoter, a 400 bp region was identified as being responsible for downregulation by VND7. These data suggested that VND7 and VNI2 mutually regulate each other, and VNI2 expression is both positively and negatively regulated in the transcriptional cascade.