Early Development of the Spinal Cord: Retinoic Acid Signalling

Qeeret Aert^*
*Correspondence: Qeeret Aert, Department of Spine Surgery, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510000, China, Email:

Introduction

The formation of the spinal cord is a complex and tightly regulated process during embryonic development. Retinoic Acid (RA) signaling plays a crucial role in orchestrating various events that govern the patterning and differentiation of the spinal cord. This article delves into the intricate interplay between RA signaling and the early development of the spinal cord. By exploring the molecular mechanisms, spatial-temporal dynamics, and functional implications of RA-mediated processes, we provide insights into the fundamental processes that shape the embryonic spinal cord [1]. The establishment of the spinal cord during embryonic development is characterized by precise temporal and spatial control of gene expression, cellular proliferation, and differentiation. Retinoic acid, a metabolite of vitamin A, emerges as a key molecular player in this process. This article aims to illuminate the significance of retinoic acid signaling in shaping the early development of the spinal cord [2,3].

Description

Retinoic acid signaling is a highly conserved pathway that involves the conversion of retinol to retinaldehyde and subsequently to retinoic acid. These active retinoids bind to nuclear receptors, the Retinoic Acid Receptors (RARs) and Retinoid X Receptors (RXRs), forming heterodimers that regulate the transcription of target genes. The RA pathway is finely tuned by synthesizing enzymes, transporters, and catabolic enzymes. During spinal cord development, RA signaling displays spatiotemporal specificity [4]. Early in embryogenesis, RA is essential for establishing the Anterior-Posterior (A-P) axis through its gradient-dependent patterning [4]. Later, RA signaling governs the differentiation of neural progenitors into distinct neuronal subtypes along the dorsoventral axis, leading to the formation of sensory and motor neurons. RA signaling serves as a morphogen that establishes the A-P identity of spinal cord segments. It influences the expression of Hox genes, which are instrumental in specifying the segmental identity of spinal neurons. Moreover, RA signaling determines the D-V fate of neural progenitors by inducing the expression of specific transcription factors that guide cell differentiation. RA-mediated processes are critical for neurogenesis, as they promote the sequential generation of different neuronal populations. Motor neurons, interneurons, and sensory neurons are generated in distinct waves, orchestrated by the temporal modulation of RA signaling. Dysregulation of RA signaling can lead to aberrant neuronal differentiation and contribute to developmental disorders [5,6].

Conclusion

Retinoic acid signaling emerges as a master regulator in the early development of the spinal cord. Through its dynamic modulation of gene expression, patterning, and differentiation, RA shapes the embryonic spinal cord's structural and functional architecture. A comprehensive understanding of the intricate interactions within the RA pathway provides insights into both normal development and potential therapeutic avenues for developmental disorders. Recent advances in genomics and molecular biology have shed light on the complex regulatory networks that intersect with RA signaling. Further studies are warranted to unravel the crosstalk between RA and other signaling pathways and to decipher the contributions of non-coding RNAs in fine-tuning spinal cord development.

Acknowledgement

None.

Conflict of Interest

None.

References

1. Stern, Claudio D., Jeroen Charite, Jacqueline Deschamps and Denis Duboule, et al. "Head-tail patterning of the vertebrate embryo: One, two or many unresolved problems?." Int J Dev Biol 50 (2003): 3-15.

Google Scholar, Crossref, Indexed at

2. Tam, P. P. L. and R. S. P. Beddington. "The formation of mesodermal tissues in the mouse embryo during gastrulation and early organogenesis." Development 99 (1987): 109-126.

Google Scholar, Crossref, Indexed at

3. Brown, Jennifer M. and Kate G. Storey. "A region of the vertebrate neural plate in which neighbouring cells can adopt neural or epidermal fates." Curr Biol 10 (2000): 869-872.

Google Scholar, Crossref, Indexed at

4. Mathis, Luc, Paul M. Kulesa and Scott E. Fraser. "FGF receptor signalling is required to maintain neural progenitors during Hensen's node progression." Nat Cell Biol 3 (2001): 559-566.

Google Scholar, Crossref, Indexed at

5. Wilson, Valerie, Isabel Olivera-Martinez and Kate G. Storey. "Stem cells, signals and vertebrate body axis extension." (2009): 1591-1604.

Google Scholar, Crossref, Indexed at

6. Dersch, Helen and Maija H. Zile. "Induction of normal cardiovascular development in the vitamin A-deprived quail embryo by natural retinoids." Dev Biol 160 (1993): 424-433.

Google Scholar, Crossref, Indexed at