UV‐B Irradiation Results in Inhibition of Hypocotyl Elongation, Cell Cycle Arrest, and Decreased Endoreduplication Mediated by miR5642. (28th December 2021)

• Record Type: Journal Article
• Authors: Dukowic‐Schulze, Stefanie; Harvey, Allison; Garcia, Nelson; Chen, Changbin; Gardner, Gary
• Is Part Of: Photochemistry and photobiology. Volume 98:Number 5(2022)
• Page Start: 1084
• Page End: 1099
• Publication Date: 2021-12-28
• Subjects: Photochemistry -- Periodicals; Light -- Physiological effect -- Periodicals; 541.35
• DOI: 10.1111/php.13574
• Languages: English
• ISSNs: 0031-8655

Abstract

ABSTRACT: UV‐B as a component of natural solar radiation can induce damage and morphological development in plants. The UV‐B response from germination and early development in seedlings is still largely unknown, with most studies focused on older, light‐exposed seedlings. We used fluence response curves measuring hypocotyl length after UV‐B exposure coupled with RNA‐seq and sRNA‐seq evaluation of the early seedling response in the model organism Arabidopsis thaliana . We identified miR5642 as a potential novel key regulator of UV‐B responses. miR5642 is a noncanonical miRNA predicted to target previously known and unknown components involved in hypocotyl growth inhibition. These include (i) SMAX1, a signal transmitter for seedling germination and growth; (ii) ZAT1, an uncharacterized transcription factor; and (iii) membrane pores and transporters (VHA‐E1, VHA‐E3, EPSIN‐LIKE and PIP1.4) implicated in cell elongation. In addition, HY5 and HYH, two homologous and redundant transcription factors involved in seedling photomorphogenesis, may interact with these newly identified components. Interestingly, UV‐B–induced DNA photodimer formation seems to be the direct trigger leading to inhibition of hypocotyl growth through a combination of cellular decisions including cell cycle arrest, reduced endoreduplication and reduced cell elongation, and this inhibition appears to be modulated by miR5642 target genes. Abstract : In the dark, UV‐B–induced DNA damage cannot be repaired via the light repair pathway, and thus, photodamage accumulates, followed by repair and cell cycle arrest. In parallel, photomorphogenesis occurs, as shown here via the small RNA miR5642. The amount of miRNA5642 increases with increasing UV‐B dosage. Identified miR5642 target genes showed decreased gene expression, and mutants had defects in UV‐B–induced inhibition of hypocotyl elongation.