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Summary: Arabidopsis MYC2 bHLH transcription factor plays a negative regulatory role in blue light (BL)‐mediated seedling development. HY5 bZIP protein works as a positive regulator of multiple wavelengths of light and promotes photomorphogenesis. Both MYC2 and HY5, belonging to two different classes of transcription factors, are the integrators of multiple signaling pathways. However, the functional interrelations of these two transcription factors in seedling development remain unknown. Additionally, whereas HY5‐mediated regulation of gene expression has been investigated in detail, the transcriptional regulation of HY5 itself is yet to be understood. Here, we show that HY5 and MYC2 work in an antagonistic manner in Arabidopsis seedling development. Our results reveal that HY5 expression is negatively regulated by MYC2 predominantly in BL, and at various stages of development. On the other hand, HY5 negatively regulates the expression of MYC2 at various wavelengths of light. In vitro and in vivo DNA–protein interaction studies suggest that MYC2 binds to the E‐box cis‐acting element of HY5 promoter. Collectively, this study demonstrates a coordinated regulation of MYC2 and HY5 in blue‐light‐mediated Arabidopsis seedling development. Significance Statement: The functional inter‐regulation of three transcription factors, MYC2, HY5 and CAM7, remains unknown in Arabidopsis seedling development. This study demonstrates a mechanistic view on coordinated regulation of these proteins in Arabidopsis seedling development. [ABSTRACT FROM AUTHOR]

Leaf chloroplast movement is thought to optimize light capture and to minimize photodamage. To better understand the impact of chloroplast movement on photosynthesis, we developed a technique based on the imaging of reflectance from leaf surfaces that enables continuous, high-sensitivity, non-invasive measurements of chloroplast movement in multiple intact plants under white actinic light. We validated the method by measuring photorelocation responses in Arabidopsis chloroplast division mutants with drastically enlarged chloroplasts, and in phototropin mutants with impaired photorelocation but normal chloroplast morphology, under different light regimes. Additionally, we expanded our platform to permit simultaneous image-based measurements of chlorophyll fluorescence and chloroplast movement. We show that chloroplast division mutants with enlarged, less-mobile chloroplasts exhibit greater photosystem II photodamage than is observed in the wild type, particularly under fluctuating high levels of light. Comparison between division mutants and the severe photorelocation mutant phot1-5 phot2-1 showed that these effects are not entirely attributable to diminished photorelocation responses, as previously hypothesized, implying that altered chloroplast morphology affects other photosynthetic processes. Our dual-imaging platform also allowed us to develop a straightforward approach to correct non-photochemical quenching ( NPQ) calculations for interference from chloroplast movement. This correction method should be generally useful when fluorescence and reflectance are measured in the same experiments. The corrected data indicate that the energy-dependent ( qE) and photoinhibitory ( qI) components of NPQ contribute differentially to the NPQ phenotypes of the chloroplast division and photorelocation mutants. This imaging technology thus provides a platform for analyzing the contributions of chloroplast movement, chloroplast morphology and other phenotypic attributes to the overall photosynthetic performance of higher plants. [ABSTRACT FROM AUTHOR]

MYC2 is a basic helix‐loop‐helix transcription factor that acts as a repressor of blue light‐mediated photomorphogenic growth; however, it promotes lateral root formation. MYC2 also regulates different phytohormone‐signaling pathways in crucial manner. Arabidopsis response regulator 16 (ARR16) is a negative regulator of cytokinin signaling pathways. Here, we show that MYC2 directly binds to the E‐box of ARR16 minimal promoter and negatively regulates its expression in a cytokinin‐dependent manner. While ARR16 and MYC2 influence jasmonic acid and cytokinin signaling, the expression of ARR16 is regulated by cry1, GBF1, and HYH, the components of light signaling pathways. The transgenic studies show that the expression of ARR16 is regulated by MYC2 at various stages of development. The mutational studies reveal that ARR16 positively regulates the hypocotyl growth in blue light, and phenotypic analysis of atmyc2 arr16 double mutant further reveals that arr16 can suppress the short hypocotyl phenotype of atmyc2. Altogether, this work highlights MYC2‐mediated transcriptional repression of ARR16 in Arabidopsis seedling development. [ABSTRACT FROM AUTHOR]

The unique member of the calmodulin gene family, Calmodulin7 (CAM7), plays a crucial role as transcriptional regulator to promote Arabidopsis seedling development. CAM7 regulates the expression of HY5, which is intimately involved in the promotion of photomorphogenic growth and light‐regulated gene expression. COP1 ubiquitin ligase suppresses photomorphogenesis by degrading multiple photomorphogenesis promoting factors including HY5 in darkness. Genetic interaction studies, in this report, reveal that CAM7 and COP1 co‐ordinately work to promote photomorphogenic growth and light‐regulated gene expression at lower intensity of light. CAM7 physically interacts with COP1 in the nucleus. Further, in vivo study suggests that CAM7 and COP1 interaction is light intensity dependent. We have also shown that functional COP1 is required for optimum accumulation of CAM7 at lower fluences of light. Taken together, this study demonstrates the coordinated function of CAM7 and COP1 in Arabidopsis seedling development. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor regarding the increased incidences of electroencephalogram (EEG) abnormalities in patients with affective disorders. Potential to differentiate subgroups with particular symptoms through EEG variations; Link between EEG abnormalities and non-familial bipolar cases; Correlation between electrical injury to the central nervous system and loss of alpha rhythms.