OsUGE2 Regulates Plant Growth through Affecting ROS Homeostasis and Iron Level in Rice

Background The growth and development of rice ( Oryza sativa  L.) are affected by multiple factors, such as ROS homeostasis and utilization of iron. Here, we demonstrate that OsUGE2 , a gene encoding a UDP-glucose 4-epimerase, controls growth and development by regulating reactive oxygen species (RO...

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Veröffentlicht in:Rice (New York, N.Y.) N.Y.), 2024-12, Vol.17 (1), p.6-6, Article 6
Hauptverfasser: Yang, Shuaiqi, Chen, Nana, Qi, Jiaxuan, Salam, Abdul, Khan, Ali Raza, Azhar, Wardah, Yang, Chunyan, Xu, Nuo, Wu, Junyu, Liu, Yihua, Liu, Bohan, Gan, Yinbo
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Sprache:eng
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Zusammenfassung:Background The growth and development of rice ( Oryza sativa  L.) are affected by multiple factors, such as ROS homeostasis and utilization of iron. Here, we demonstrate that OsUGE2 , a gene encoding a UDP-glucose 4-epimerase, controls growth and development by regulating reactive oxygen species (ROS) and iron (Fe) level in rice. Knockout of this gene resulted in impaired growth, such as dwarf phenotype, weakened root growth and pale yellow leaves. Biochemical analysis showed that loss of function of OsUGE2 significantly altered the proportion and content of UDP-Glucose (UDP-Glc) and UDP-Galactose (UDP-Gal). Cellular observation indicates that the impaired growth may result from decreased cell length. More importantly, RNA-sequencing analysis showed that knockout of OsUGE2 significantly influenced the expression of genes related to oxidoreductase process and iron ion homeostasis. Consistently, the content of ROS and Fe are significantly decreased in OsUGE2 knockout mutant. Furthermore, knockout mutants of OsUGE2 are insensitive to both Fe deficiency and hydrogen peroxide (H 2 O 2 ) treatment, which further confirmed that OsUGE2 control rice growth possibly through Fe and H 2 O 2 signal. Collectively, these results reveal a new pathway that OsUGE2 could affect growth and development via influencing ROS homeostasis and Fe level in rice.
ISSN:1939-8425
1939-8433
1934-8037
DOI:10.1186/s12284-024-00685-0