BIN2

Last update 08 May 2025

Basic Info

Synonyms

BIN2, BRAP-1, BRAP1

+ [2]

Introduction

Promotes cell motility and migration, probably via its interaction with the cell membrane and with podosome proteins that mediate interaction with the cytoskeleton. Modulates membrane curvature and mediates membrane tubulation. Plays a role in podosome formation. Inhibits phagocytosis.

100 Clinical Results associated with BIN2

100 Translational Medicine associated with BIN2

0 Patents (Medical) associated with BIN2

184

Literatures (Medical) associated with BIN2

01 Apr 2025·Plant Molecular Biology

A glycogen synthase kinase-3 gene enhances grain yield heterosis in semi-dwarf rapeseed

Article

Author: Liang, Qu ; Mei, Li ; Qian, Yang ; Bao, Li ; Lichao, Deng ; Yiming, Guo ; Xinhong, Liu ; Hui, Zhang ; Wenqing, Tan ; Mingli, Yan

Optimizing plant height is a key breeding objective in Brassica napus to enhance lodging resistance and increase yield potential. In the present study, we identified a semi-dwarf gene in rapeseed, BnDWARF5 (BnDF5), which encodes a glycogen synthase kinase 3, BRASSINOSTEROID-INSENSITIVE 2 (BnaC03.BIN2), primarily controlling the elongation of basal internodes by inhibiting the elongation of internode cells. Genetic mapping and cloning revealed that BnDF5 is governed by a semi-dominant/dominant gene located on chromosome C03. Sequencing uncovered an SNP in BnaC03.BIN2 due to an amino acid substitution, which was confirmed via kompetitive allele-specific polymerase chain reaction marker analysis, and expressing the mutated BnaC03.BIN2 in the wild type resulted in decreased plant height. Practical breeding applications showed that heterozygous BnDF5 plants exhibited optimal intermediate height and strong yield heterosis, making the semi-dwarf mutant a valuable genetic resource for developing semi-dwarf rapeseed varieties with improved lodging resistance and yield.

01 Apr 2025·Molecular Plant

FERONIA signaling maintains cell wall integrity during brassinosteroid-induced cell expansion in Arabidopsis

Article

Author: Malkovskiy, Andrey ; Wu, Hen-Ming ; Cheung, Alice Y ; Župunski, Milan ; Zhang, Hongliang ; Hsiao, Yu-Chun ; Aizezi, Yalikunjiang ; Chaudhary, Ajeet ; Wang, Zhi-Yong ; Grossmann, Guido ; Xu, Shou-Ling ; Jessica Yeh, Fang-Ling

Plant cell expansion is regulated by hormones and driven by turgor pressure, which stretches the cell wall and can potentially cause wall damage or rupture. How plant cells avoid cell wall rupture during hormone-induced rapid cell expansion remains poorly understood. Here, we show that the wall-sensing receptor kinase FERONIA (FER) plays an essential role in maintaining cell wall integrity during brassinosteroid (BR)-induced cell elongation. Compared with the wild type, the BR-treated fer mutants display an increased initial acceleration of cell elongation, increased cell wall damage and rupture, reduced production of reactive oxygen species (ROS), and enhanced cell wall acidification. Long-term treatments of fer with high concentrations of BR cause stress responses and reduce growth, whereas osmolytes, reducing turgor, alleviate the defects. These results show that BR-induced cell elongation causes damage to cell walls and the release of cell wall fragments that activate FER, which promotes ROS production, attenuates apoplastic acidification, and slows cell elongation, thereby preventing further cell wall damage and rupture. Furthermore, we show that BR signaling promotes FER accumulation at the plasma membrane (PM). When the BR level is low, the GSK3-like kinase BIN2 phosphorylates FER to reduce FER accumulation and translocation from the endoplasmic reticulum to PM. BR-induced inactivation of BIN2 leads to dephosphorylation and PM accumulation of FER. Thus, BR signaling enhances FER-mediated cell wall integrity surveillance while promoting cell expansion, whereas FER acts as a brake to maintain a safe cell elongation rate. Collectively, our study reveals a vital signaling circuit that coordinates hormone signaling with mechanical sensing to prevent cell rupture during hormone-induced cell expansion.

01 Feb 2025·Journal of Integrative Plant Biology

Dual regulation of stomatal development by brassinosteroid in Arabidopsis hypocotyls

Article

Author: Ko, Yeong‐Woo ; Kim, Tae‐Wuk ; Park, Tae‐Ki ; Oh, Eunkyoo ; Kim, Yun Ju ; Kim, So‐Hee ; Lee, Se‐Hwa

ABSTRACTStomata are epidermal pores that are essential for water evaporation and gas exchange in plants. Stomatal development is orchestrated by intrinsic developmental programs, hormonal controls, and environmental cues. The steroid hormone brassinosteroid (BR) inhibits stomatal lineage progression by regulating BIN2 and BSL proteins in leaves. Notably, BR is known to promote stomatal development in hypocotyls as opposed to leaves; however, its molecular mechanism remains elusive. Here, we show that BR signaling has a dual regulatory role in controlling stomatal development in Arabidopsis hypocotyls. We found that brassinolide (BL; the most active BR) regulates stomatal development differently in a concentration‐dependent manner. At low and moderate concentrations, BL promoted stomatal formation by upregulating the expression of SPEECHLESS (SPCH) and its target genes independently of BIN2 regulation. In contrast, high concentrations of BL and bikinin, which is a specific inhibitor of BIN2 and its homologs, significantly reduced stomatal formation. Genetic analyses revealed that BIN2 regulates stomatal development in hypocotyls through molecular mechanisms distinct from the regulatory mechanism of the cotyledons. In hypocotyls, BIN2 promoted stomatal development by inactivating BZR1, which suppresses the expression of SPCH and its target genes. Taken together, our results suggest that BR precisely coordinates the stomatal development of hypocotyls using an antagonistic control of SPCH expression via BZR1‐dependent and BZR1‐independent transcriptional regulation.

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