Dissection of the microProtein miP1 floral repressor complex in Arabidopsis

Rodrigues, V. L.; Dolde, U.; Straub, D.; Eguen, T.; Botterweg-Paredes, E.; Sun, B.; Hong, S.; Graeff, M.; Li, M.-W.; Gendron, J.; Wenkel, S.

doi:10.1101/258228

bioRxiv · 10.1101/258228

Dissection of the microProtein miP1 floral repressor complex in Arabidopsis

Rodrigues, V. L.·Dolde, U.·Straub, D.·Eguen, T.·Botterweg-Paredes, E.·Sun, B.·Hong, S.·Graeff, M.·Li, M.-W.·Gendron, J.·Wenkel, S.

View original source ↗Export metadata ↓

Abstract

MicroProteins have emerged as potent regulators of transcription factor activity. Here we use a combination of forward genetics and proteomics to dissect the miP1a/b microProtein complex that acts to delay the floral transition in Arabidopsis. The microProteins miP1a and miP1b can bridge an interaction between the flowering promoting factor CONSTANS (CO) and the TOPLESS (TPL) co-repressor protein to represses flowering. We find that the JUMONJI14 (JMJ14) histone demethylase is part of this repressor complex that can initiate chromatin changes in FLOWERING LOCUS T (FT) gene, the direct target of CO. Plants with mutations in JMJ14 exhibit an early flowering phenotype that is largely dependent on the activity of CO, supporting a role for CO in this repressive complex. When mis-expressed at the shoot apex, CO can induce early flowering only in the jmj14 background. Our results indicate that the repressor acts in the shoot apical meristem to keep it in an undifferentiated state until the leaf-derived florigen signal induces the conversion into a floral meristem.

Explore related subjects

plant biology Preprint

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

Rodrigues, V. L., Dolde, U., Straub, D., Eguen, T., Botterweg-Paredes, E., Sun, B., Hong, S., Graeff, M., Li, M.-W., Gendron, J., Wenkel, S.. 2018-02-01. Dissection of the microProtein miP1 floral repressor complex in Arabidopsis. https://doi.org/10.1101/258228

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

The genetic basis of extra-lobed leaves in ivyleaf morning glory (Ipomoea hederacea)

Intraspecific leaf shape variation is common among angiosperms. Ivyleaf morning glory (Ipomoea hederacea) has become a useful system for studying the genetics and ecology of leaf shape variation as this species exhibits two leaf shapes: leaves with entire margins, and 3-lobed leaves. It is known that these phenotypes are controlled by a single locus, and differ in their ecophysiology, geographic distribution, ecology, and fitness. However, individuals producing leaves with 1-2 extra lobes have also been observed, but the genetic basis of these phenotypes have not been described. To investigate the genetic basis of extra-lobing, we compared phenotypic distributions of leaf shapes of an F2 generation to Mendelian ratios for a single locus trait, and conducted a bulked segregant analysis to uncover quantitative trait loci. Our results suggest that producing extra-lobed leaves has a complex genetic basis and that there are multiple QTLs underlying this phenotype containing potential candidate genes involved with auxin distribution and leaf development. Whether these extra-lobed phenotypes also differ in terms of their physiology and ecology remains unexplored.

plant biology↗

bioRxiv2026

The GSNOR1-VDAC3 complex acts as a cargo co-receptor for mitophagy in response to mitochondrial stress in plants

Mitochondria are central for cellular energy metabolism, and their quality is warranted by multiple mechanisms, including mitophagy, a process of selectively removing damaged, aged, or excess mitochondria. However, the regulatory mechanism of mitophagy remains elusive in plants. Here, we report that Arabidopsis S-nitrosoglutathione reductase 1 (GSNOR1), an enzyme that has long been known to degrade S-nitrosoglutathione, interacts with the outer mitochondrial membrane protein Voltage-Dependent Anion Channel 3 (VDAC3) to mediate mitophagy. GSNOR1 translocates to depolarized mitochondria, binds to VDAC3, and interacts with Autophagy-related 8 (ATG8) via its ATG8-interacting motifs, thereby engulfing damaged mitochondria in autophagosomes for mitophagic degradation. Mutations in GSNOR1 or VDAC3 cause the accumulation of misshapen mitochondria and hypersensitivity to mitochondrial stress. We propose that GSNOR1 acts as a cargo receptor interacting with VDAC3 and ATG8 to target depolarized mitochondria to mitophagy, thereby regulating cellular homeostasis.

plant biology↗

bioRxiv2026

Ontogenetic and time-course transcriptomic analyses of maize leaf primordia reveal regulators of transverse vein development

Leaf vein patterning varies greatly among land plants and is linked to leaf structure and function. C4 plants, such as maize, have a denser arrangement of veins than C3 plants, which is hypothesized to be a pre-adaptive trait for C4 photosynthesis. Therefore, understanding how leaf veins are patterned has implications for maximizing photosynthetic efficiency. Major maize leaf veins, called longitudinal veins, are arranged in parallel and are interconnected by transverse veins. Recent work has established molecular factors controlling longitudinal vein development; however, it is unknown how transverse veins are patterned. Here, we investigated how transverse veins establish connections within the maize vascular network. We performed anatomical analyses of transverse veins and found that despite asynchronous development, transverse veins fully integrate into the longitudinal vein network. Tracing the ontogeny of transverse vein development using the marker PIN1a-YFP, we found that two sets of two initial cells on opposing sides of adjacent longitudinal veins recruit intervening ground cells to form the provascular strand. Treatment with auxin inhibitors did not abolish transverse vein initiation, suggesting an auxin-independent pre-pattern for transverse vein initiation. Through time-course RNAseq of leaf primordia, we identified a transcriptional signature that precedes transverse vein development. Two genes that belong to this gene cluster, EREB41 and EREB114, are necessary for transverse vein formation. Together, our studies establish the ontogeny of maize transverse vein development and reveal how new vascular connections are specified, assembled, and integrated into an existing vascular network.

plant biology↗