miR-216a regulates snx5, a novel notch signaling pathway component, during zebrafish retinal development

Olena, Abigail F.; Rao, Mahesh; Thatcher, Elizabeth J.; Wu, Shu-Yu; Patton, James G.

doi:10.1016/j.ydbio.2015.01.016

Cited by 30 publications

(27 citation statements)

References 57 publications

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“…This is supported by the fact that injection of gabazine or NBQX causes an upregulation of the Notch reporter Her4, suggesting that GABA is upstream of Notch signaling. This is also in line with earlier studies showing that Notch signaling is important for later stages of regeneration and development (Hayes et al., 2007, Karl et al., 2008, Kassen et al., 2007, Olena et al., 2015, Raymond et al., 2006). In addition, leptin mRNA was observed to increase following injury, suggesting that it is induced by some other signal.…”

Section: Discussionmentioning

confidence: 99%

Neurotransmitter-Regulated Regeneration in the Zebrafish Retina

2017

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SummaryCurrent efforts to repair damaged or diseased mammalian retinas are inefficient and largely incapable of fully restoring vision. Conversely, the zebrafish retina is capable of spontaneous regeneration upon damage using Müller glia (MG)-derived progenitors. Understanding how zebrafish MG initiate regeneration may help develop new treatments that prompt mammalian retinas to regenerate. We show that inhibition of γ-aminobutyric acid (GABA) signaling facilitates initiation of MG proliferation. GABA levels decrease following damage, and MG are positioned to detect decreased ambient levels and undergo dedifferentiation. Using pharmacological and genetic approaches, we demonstrate that GABAA receptor inhibition stimulates regeneration in undamaged retinas while activation inhibits regeneration in damaged retinas.

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Section: Discussionmentioning

confidence: 99%

Neurotransmitter-Regulated Regeneration in the Zebrafish Retina

2017

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“…Separation of total proteins and transfer was performed as described (Olena et al, 2015). The following antibodies were used for western blots: rabbit anti-GFP (1:1000, Torrey Pines), rabbit anti-α-tubulin (1:1000, Abcam), mouse anti-FAK (1:300, H-1 Santa Cruz Biotechnology), mouse anti-GAPDH (1:20,000, Ambion), anti-rabbit and anti-mouse HRP-conjugated secondary antibodies (1:5000, GE Healthcare).…”

Section: Methodsmentioning

confidence: 99%

“…Hybridized probes were detected using anti-digoxigenin alkaline-phosphatase conjugated antibodies, followed by incubation with nitro blue tetrazolium chloride and 5-bromo-4-chloro-3-indolyl-phosphate (NBT/BCIP) solution (Roche Applied Sciences). Whole-mount miRNA in situ hybridization was performed as described (Olena et al, 2015) using miRCURY 5′-and 3′-DIG labeled LNA (locked nucleic acid) probes (Exiqon). LNA probe #: dre-miR-27a: 613249-360; dre-miR-27b: 613734-360; dre-miR-27c-3p: 613613-360.…”

Section: Methodsmentioning

confidence: 99%

miR-27 regulates chondrogenesis by suppressing focal adhesion kinase during pharyngeal arch development

Kara

Wei

Commanday

et al. 2017

Developmental Biology

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Cranial neural crest cells are a multipotent cell population that generate all the elements of the pharyngeal cartilage with differentiation into chondrocytes tightly regulated by temporal intracellular and extracellular cues. Here, we demonstrate a novel role for miR-27, a highly enriched microRNA in the pharyngeal arches, as a positive regulator of chondrogenesis. Knock down of miR-27 led to nearly complete loss of pharyngeal cartilage by attenuating proliferation and blocking differentiation of pre-chondrogenic cells. Focal adhesion kinase (FAK) is a key regulator in integrin-mediated extracellular matrix (ECM) adhesion and has been proposed to function as a negative regulator of chondrogenesis. We show that FAK is downregulated in the pharyngeal arches during chondrogenesis and is a direct target of miR-27. Suppressing the accumulation of FAK in miR-27 morphants partially rescued the severe pharyngeal cartilage defects observed upon knock down of miR-27. These data support a crucial role for miR-27 in promoting chondrogenic differentiation in the pharyngeal arches through regulation of FAK.

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“…Snx5 co-localizes with mindbomb in endosomal compartments and is important for its trafficking and thus formation of mindbomb/delta complexes [35]. The microRNA miR-216a is expressed in a complimentary pattern to snx5 in the retina, and has been shown to regulate snx5 [36]. Consequently, knockdown of miR-216a results in increased Notch signaling.…”

Section: Receptor Cleavage Regulationmentioning

confidence: 99%

The Regulation of Notch Signaling in Retinal Development and Regeneration

Mills

Goldman

2017

Curr Pathobiol Rep

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Purpose of review Notch signaling is an important component of retinal progenitor cell maintenance and MG specification during development, and its manipulation may be critical for allowing MG to re-enter the cell cycle and regenerate neurons in adults. In mammals, MG respond to retinal injury by undergoing a gliotic response rather than a regenerative one. Understanding the complexities of Notch signaling may allow for strategies that enhance regeneration over gliosis. Recent findings Notch signaling is regulated at multiple levels, and is interdependent with various other signaling pathways in both the receptor and ligand expressing cells. The precise spatial and temporal patterning of Notch components is necessary for proper retinal development. Regenerative species undergo a dynamic regulation of Notch signaling in MG upon injury, whereas non-regenerative species fail to productively regulate Notch. Summary Notch signaling is malleable, such that the altered composition of growth and transcription factors in the developing and mature retinas result in different Notch mediated responses. Successful regeneration will require the manipulation of the retinal environment to foster a dynamic rather than static regulation of Notch signaling in concert with other reprogramming and differentiation factors.

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miR-216a regulates snx5, a novel notch signaling pathway component, during zebrafish retinal development

Cited by 30 publications

References 57 publications

Neurotransmitter-Regulated Regeneration in the Zebrafish Retina

Neurotransmitter-Regulated Regeneration in the Zebrafish Retina

miR-27 regulates chondrogenesis by suppressing focal adhesion kinase during pharyngeal arch development

The Regulation of Notch Signaling in Retinal Development and Regeneration

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