Olig3 is not involved in the ventral patterning of spinal cord.

Zijing Liu,Xuemei Hu,Mengsheng Qiu,Chengcheng Huang,Cheng Cao,Kang Zheng,Hirohide Takebayashi,Brahim Nait-Oumesmar

doi:10.1371/journal.pone.0111076

Zijing Liu, Xuemei Hu + Show 6 more

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https://doi.org/10.1371/journal.pone.0111076

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Abstract

At embryonic stages, Olig3 is initially expressed in the dorsal-most region of the spinal cord, but later in the ventral marginal zone as well. Previous studies indicated that Olig3 controlled the patterning of dorsal spinal cord and loss of Olig3 function led to the re-specification of dI2 and dI3 neurons into dI4 interneurons. However, the role of Olig3 in regulating the development of ventral spinal cord has remained unknown. BrdU labeling demonstrated that ventral Olig3 was expressed in the post-mitotic neurons and Olig3+ cells seen at late embryonic stages were born at the earlier stage but remained in the marginal zone throughout embryogenesis. Loss-of-function and gain-of-function experiment indicated that Nkx2.2 regulated the expression of Olig3 in V3 interneurons. However, Olig3 mutation didn’t apparently affect the generation and migration of ventral neurons. These findings suggest that Olig3 plays different roles in regulating the development of dorsal and ventral spinal cord.

Highlights

In the past few years, considerable progress has been made in understanding the patterning of the spinal cord ventricular zone
Expression pattern in embryonic spinal cord As a first step to elucidate the function of Olig3 in spinal neurogenesis, we carried out detailed analysis on Olig3 expression in embryonic chick spinal cord at various development stages
Starting at cE4, Olig3 expression was detected in the marginal zone at the intermediate and ventral-most regions of spinal cord, whereas dorsal Olig3 expression was observed in a broad region (Figure 1B)

Summary

Introduction

In the past few years, considerable progress has been made in understanding the patterning of the spinal cord ventricular zone. The ventral ventricular zone can be divided into five distinct domains (p0–p3 and pMN), each of which generates a unique neuronal type [4,5]. Olig and Olig are selectively expressed in pMN domain and play key roles in controlling the specification of both motor neurons and oligodendrocytes in the spinal cord. Loss of Olig in mutant completely inhibited the generation of motor neurons and oligodendrocyte, whereas Olig knockout mice showed the delay of oligodendrocyte differentiation [6,7,8]. Previous studies showed that Olig was involved in the patterning of dorsal spinal cord and hindbrain [11,12,13]. In Olig mutant hindbrain, the generation of inferior olive nucleus, nucleus of the solitary tract and brainstem (nor)adrenergic centers is completely inhibited, but the formation of four mossy-fiber nuclei is reduced [11]

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