DIP2B Interacts With α-Tubulin to Regulate Axon Outgrowth

Xing, Zhenkai; Zhang, Luqing; Sun, Xue; Sun, Xin; Yu, Huali; Zheng, Yaowu; He, Zixuan; Zhu, Xinen

doi:10.3389/fncel.2020.00029

Cited by 12 publications

(13 citation statements)

References 34 publications

(36 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These expression results indicate that Dip2b may play a role in neurogenesis. This is supported, in part, by our recent studies on Dip2b expression and its potential role during neurite outgrowth in Dip2b tm1a/tm1a hippocampal cultured cell [25]. A previous report suggested that Dip2b may play a role in mental retardation and in schizophrenia [3,12].…”

Section: Discussionsupporting

confidence: 72%

See 1 more Smart Citation

Analysis of Dip2B Expression in Adult Mouse Tissues Using the LacZ Reporter Gene

Sah

Bahadar

Adlat

et al. 2021

CIMB

View full text Add to dashboard Cite

Disconnected (disco)-interacting protein 2 homolog B (Dip2B) is a member of the Dip2 superfamily and plays an essential role in axonal outgrowth during embryogenesis. In adults, Dip2B is highly expressed in different brain regions, as shown by in situ analysis, and may have a role in axon guidance. However, the expression and biological role of Dip2B in other somatic tissues remain unknown. To better visualize Dip2B expression and to provide insight into the roles of Dip2B during postnatal development, we used a Dip2btm1a(wtsi)komp knock-in mouse model, in which a LacZ-Neo fusion protein is expressed under Dip2b promoter and allowed Dip2B expression to be analyzed by X-gal staining. qPCR analyses showed that Dip2b mRNA was expressed in a variety of somatic tissues, including lung and kidney, in addition to brain. LacZ staining indicated that Dip2B is broadly expressed in neuronal, reproductive, and vascular tissues as well as in the kidneys, heart, liver, and lungs. Moreover, neurons and epithelial cells showed rich staining. The broad and intense patterns of Dip2B expression in adult mice provide evidence of the distribution of Dip2B in multiple locations and, thereby, its implication in numerous physiological roles.

show abstract

Section: Discussionsupporting

confidence: 72%

“…LacZ expression was also detected in the prostate gland, oocytes, kidneys, adrenal glands, and intestinal glands. Cytological investigations are ongoing to identify the cell type-specific distribution of Dip2b gene expression and to elucidate possible functions of the Dip2b gene in these organs [16,25].…”

Section: Discussionmentioning

confidence: 99%

Analysis of Dip2B Expression in Adult Mouse Tissues Using the LacZ Reporter Gene

Sah

Bahadar

Adlat

et al. 2021

CIMB

View full text Add to dashboard Cite

show abstract

“…Mammalian DIP2B has been implicated in neuronal tubulin acetylation in axon outgrowth 26 . The specific function of DIP2 family members in neuronal lipid organization or membrane architecture is not known, and the relationship of DIP2 to other morphology maintenance pathways remains poorly understood.…”

Section: Dip2 Proteins Function In Neuronal Morphology Maintenance An...mentioning

confidence: 99%

Dopey-dependent regulation of extracellular vesicles maintains neuronal morphology

Park,

Noblett,

Pitts

et al. 2024

Preprint

View full text Add to dashboard Cite

Mature neurons maintain their distinctive morphology for extended periods in adult life. Compared to developmental neurite outgrowth, axon guidance, and target selection, relatively little is known of mechanisms that maintain mature neuron morphology. Loss of function in C. elegans DIP-2, a member of the conserved lipid metabolic regulator Dip2 family, results in progressive overgrowth of neurites in adults. We find that dip-2 mutants display specific genetic interactions with sax-2, the C. elegans ortholog of Drosophila Furry and mammalian FRY. Combined loss of DIP-2 and SAX-2 results in severe disruption of neuronal morphology maintenance accompanied by increased release of neuronal extracellular vesicles (EVs). By screening for suppressors of dip-2 sax-2 double mutant defects we identified gain-of-function (gf) mutations in the conserved Dopey family protein PAD-1 and its associated phospholipid flippase TAT-5/ATP9A. In dip-2 sax-2 double mutants carrying either pad-1(gf) or tat-5(gf) mutation, EV release is reduced and neuronal morphology across multiple neuron types is restored to largely normal. PAD-1(gf) acts cell autonomously in neurons. The domain containing pad-1(gf) is essential for PAD-1 function, and PAD-1(gf) protein displays increased association with the plasma membrane and inhibits EV release. Our findings uncover a novel functional network of DIP-2, SAX-2, PAD-1, and TAT-5 that maintains morphology of neurons and other types of cells, shedding light on the mechanistic basis of neurological disorders involving human orthologs of these genes.

show abstract

“…However, in individuals where both FRA12A and ID were present, DIP2B expression was reduced to half that of controls [ 33 ]. DIP2B has been determined to be a regulator of axonal development and is essential for the development of neuron cells [ 66 ]. Therefore, if DIP2B were to be transcriptionally silenced in a large proportion of cells during early neuronal development this may be a contributing mechanism towards neurocognitive disorders.…”

Section: Fra12a — Dip2bmentioning

confidence: 99%

Unravelling the link between neurodevelopmental disorders and short tandem CGG-repeat expansions

Annear,

Kooy

2023

Emerging Topics in Life Sciences

View full text Add to dashboard Cite

Neurodevelopmental disorders (NDDs) encompass a diverse group of disorders characterised by impaired cognitive abilities and developmental challenges. Short tandem repeats (STRs), repetitive DNA sequences found throughout the human genome, have emerged as potential contributors to NDDs. Specifically, the CGG trinucleotide repeat has been implicated in a wide range of NDDs, including Fragile X Syndrome (FXS), the most common inherited form of intellectual disability and autism. This review focuses on CGG STR expansions associated with NDDs and their impact on gene expression through repeat expansion-mediated epigenetic silencing. We explore the molecular mechanisms underlying CGG-repeat expansion and the resulting epigenetic modifications, such as DNA hypermethylation and gene silencing. Additionally, we discuss the involvement of other CGG STRs in neurodevelopmental diseases. Several examples, including FMR1, AFF2, AFF3, XYLT1, FRA10AC1, CBL, and DIP2B, highlight the complex relationship between CGG STR expansions and NDDs. Furthermore, recent advancements in this field are highlighted, shedding light on potential future research directions. Understanding the role of STRs, particularly CGG-repeats, in NDDs has the potential to uncover novel diagnostic and therapeutic strategies for these challenging disorders.

show abstract

DIP2B Interacts With α-Tubulin to Regulate Axon Outgrowth

Cited by 12 publications

References 34 publications

Analysis of Dip2B Expression in Adult Mouse Tissues Using the LacZ Reporter Gene

Analysis of Dip2B Expression in Adult Mouse Tissues Using the LacZ Reporter Gene

Dopey-dependent regulation of extracellular vesicles maintains neuronal morphology

Unravelling the link between neurodevelopmental disorders and short tandem CGG-repeat expansions

Contact Info

Product

Resources

About