Early Development of the Spiral Ganglion

Goodrich, Lisa V.

doi:10.1007/978-1-4939-3031-9_2

Cited by 31 publications

(33 citation statements)

References 181 publications

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“…However, we cannot exclude that the more numerous type I afferents also show unusual branching in the apex. To our knowledge, such unusual branches have not been described before in investigations of normal type II development [47, 48, 61]. A somewhat similar phenotype has previously been described in Prox1 mutants with a conditional deletion restricted to spiral ganglion neurons that may be increased by the Prox1 expression in supporting cells [62].…”

Section: Discussionsupporting

confidence: 61%

Prickle1 regulates neurite outgrowth of apical spiral ganglion neurons but not hair cell polarity in the murine cochlea

Yang

Kersigo

et al. 2017

PLoS ONE

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In the mammalian organ of Corti (OC), the stereocilia on the apical surface of hair cells (HCs) are uniformly organized in a neural to abneural axis (or medial-laterally). This organization is regulated by planar cell polarity (PCP) signaling. Mutations of PCP genes, such as Vangl2, Dvl1/2, Celsr1, and Fzd3/6, affect the formation of HC orientation to varying degrees. Prickle1 is a PCP signaling gene that belongs to the prickle / espinas / testin family. Prickle1 protein is shown to be asymmetrically localized in the HCs of the OC, and this asymmetric localization is associated with loss of PCP in Smurf mutants, implying that Prickle1 is involved in HC PCP development in the OC. A follow-up study found no PCP polarity defects after loss of Prickle1 (Prickle1-/-) in the cochlea. We show here strong Prickle1 mRNA expression in the spiral ganglion by in situ hybridization and β-Gal staining, and weak expression in the OC by β-Gal staining. Consistent with this limited expression in the OC, cochlear HC PCP is unaffected in either Prickle1C251X/C251X mice or Prickle1f/f; Pax2-cre conditional null mice. Meanwhile, type II afferents of apical spiral ganglion neurons (SGN) innervating outer hair cells (OHC) have unusual neurite growth. In addition, afferents from the apex show unusual collaterals in the cochlear nuclei that overlap with basal turn afferents. Our findings argue against the role of Prickle1 in regulating hair cell polarity in the cochlea. Instead, Prickle1 regulates the polarity-related growth of distal and central processes of apical SGNs.

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Section: Discussionsupporting

confidence: 61%

Prickle1 regulates neurite outgrowth of apical spiral ganglion neurons but not hair cell polarity in the murine cochlea

Yang

Kersigo

et al. 2017

PLoS ONE

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“…Inner ear sensory neuron formation requires a series of transcription factors starting with the expression of the bHLH genes Neurog1724, Neurod143 and followed by several other factors needed to fully differentiate the neurons, guide their migration away from the ear, and process growth to the ear644. Neurons delaminate from multiple sites in the sensory epithelia or areas adjacent to the sensory epithelia such as the region between the cochlear base and the saccule1045.…”

Section: Discussionmentioning

confidence: 99%

Incomplete and delayed Sox2 deletion defines residual ear neurosensory development and maintenance

Dvorakova

Jahan

Mácová

et al. 2016

Sci Rep

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The role of Sox2 in neurosensory development is not yet fully understood. Using mice with conditional Islet1-cre mediated deletion of Sox2, we explored the function of Sox2 in neurosensory development in a model with limited cell type diversification, the inner ear. In Sox2 conditional mutants, neurons initially appear to form normally, whereas late- differentiating neurons of the cochlear apex never form. Variable numbers of hair cells differentiate in the utricle, saccule, and cochlear base but sensory epithelium formation is completely absent in the apex and all three cristae of the semicircular canal ampullae. Hair cells differentiate only in sensory epithelia known or proposed to have a lineage relationship of neurons and hair cells. All initially formed neurons lacking hair cell targets die by apoptosis days after they project toward non-existing epithelia. Therefore, late neuronal development depends directly on Sox2 for differentiation and on the survival of hair cells, possibly derived from common neurosensory precursors.

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“…However, while there is an obvious interaction of neuronal precursor formation with hair cell development (Matei et al, 2005), the detailed nature of it remains unclear at a molecular and cellular level (Jahan et al, 2015b; Raft and Groves, 2015). What is clear is the sequence of activations of transcription factors that result in proliferation of neuronal precursors and their differentiation (Goodrich, 2016). Integral to this emerging perspective are several transcription factors such as Neurod1 for normal differentiation and targeted projection to the brain and the periphery (Jahan et al, 2010a), possibly through regulation of the Pou-domain factor Brn3a (Pou4f1) and both regulate expression of neurotrophin receptors (Huang et al, 2001; Kim et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

“…Details of the molecular basis of afferent segregation in the ear and to the CNS remain obscure but may be related to several known pathfinding molecules such Ephrins (Cramer and Gabriele, 2014; Siddiqui and Cramer, 2005), semaphorins, and other diffusible factors released from the hindbrain such as Wnts and Bmps (Henríquez and Osses, 2016; Seiradake et al, 2016) as well as cellular interactions. Clearly, Gata3 and Neurod1 are critical for this segregated projection from the ear to the cochlear nuclei (Fritzsch et al, 2006b; Goodrich, 2016; Jahan et al, 2010a) but exactly when the relevant genes were first expressed in the auditory inner ear neurons and how they tied into the novel pathfinding selection process to connect a novel periphery with a novel central target remains to be shown (Fritzsch et al, 2015b). Consistent with the ancestral split of a neurosensory cell with an axon into a hair cell and its sensory neuron is that central projections of sensory neurons do not depend on neural crest derived Schwann cells (Mao et al, 2014) whereas the peripheral projection is highly disorganized and many afferents miss the hair cells and sensory epithelia (Fig.…”

Section: Introductionmentioning

confidence: 99%

Gene, cell, and organ multiplication drives inner ear evolution

Fritzsch

Elliott

2017

Developmental Biology

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We review the development and evolution of the ear neurosensory cells, the aggregation of neurosensory cells into an otic placode, the evolution of novel neurosensory structures dedicated to hearing and the evolution of novel nuclei and their input dedicated to processing those novel auditory stimuli. The evolution of the apparently novel auditory system lies in duplication and diversification of cell fate transcription regulation that allows variation at the cellular level [transforming a single neurosensory cell into a sensory cell connected to its targets by a sensory neuron as well as diversifying hair cells], organ level [duplication of organ development followed by diversification and novel stimulus acquisition] and brain nuclear level [multiplication of transcription factors to regulate various neuron and neuron aggregate fate to transform the spinal cord into the unique hindbrain organization]. Tying cell fate changes driven by bHLH and other transcription factors into cell and organ changes is at the moment tentative as not all relevant factors are known and their gene regulatory network is only rudimentary understood. Future research can use the blueprint proposed here to provide both the deeper molecular evolutionary understanding as well as a more detailed appreciation of developmental networks. This understanding can reveal how an auditory system evolved through transformation of existing cell fate determining networks and thus how neurosensory evolution occurred through molecular changes affecting cell fate decision processes. Appreciating the evolutionary cascade of developmental program changes could allow identifying essential steps needed to restore cells and organs in the future.

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Early Development of the Spiral Ganglion

Cited by 31 publications

References 181 publications

Prickle1 regulates neurite outgrowth of apical spiral ganglion neurons but not hair cell polarity in the murine cochlea

Prickle1 regulates neurite outgrowth of apical spiral ganglion neurons but not hair cell polarity in the murine cochlea

Incomplete and delayed Sox2 deletion defines residual ear neurosensory development and maintenance

Gene, cell, and organ multiplication drives inner ear evolution

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