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13 pages, 490 KB

Open AccessReview

The Development of Horns in Bovidae and the Genetic Mechanisms Underpinning This Process

by Xiaoli Xu, Wenwen Yan, Jiazhong Guo, Dinghui Dai, Li Li and Hongping Zhang

Biology 2025, 14(8), 1027; https://doi.org/10.3390/biology14081027 - 11 Aug 2025

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Horns in Bovidae, including bovines, sheep, and goats, are evolutionarily conserved cranial structures derived from cranial neural crest cells and composed of a bony core, dermis, epidermis, and keratinous sheath. Their development follows a shared trajectory across species, progressing through placode, fleshy, and mature stages. Genetic regulators such as RXFP2, FOXL2, HOXD1, and TWIST1 have been identified as pivotal determinants controlling horn morphogenesis, sexual dimorphism, and the polled phenotype. This review synthesizes current advances in the evolutionary origins, morphological progression, and genetic regulation of horn formation in bovines, sheep, and goats to provide a comprehensive understanding of horn formation and variation. These findings lay the groundwork for future efforts to manipulate horn traits through genetic selection or genome editing, with implications for animal welfare and breeding. Full article

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16 pages, 6428 KB

Open AccessFeature PaperArticle

Neurogenin 2 and Neuronal Differentiation 1 Control Proper Development of the Chick Trigeminal Ganglion and Its Nerve Branches

by Parinaz Bina, Margaret A. Hines, Johena Sanyal and Lisa A. Taneyhill

J. Dev. Biol. 2023, 11(1), 8; https://doi.org/10.3390/jdb11010008 - 19 Feb 2023

Cited by 3 | Viewed by 3176

Abstract

The trigeminal ganglion contains the cell bodies of sensory neurons comprising cranial nerve V, which relays information related to pain, touch, and temperature from the face and head to the brain. Like other cranial ganglia, the trigeminal ganglion is composed of neuronal derivatives of two critical embryonic cell types, neural crest and placode cells. Neurogenesis within the cranial ganglia is promoted by Neurogenin 2 (Neurog2), which is expressed in trigeminal placode cells and their neuronal derivatives, and transcriptionally activates neuronal differentiation genes such as Neuronal Differentiation 1 (NeuroD1). Little is known, however, about the role of Neurog2 and NeuroD1 during chick trigeminal gangliogenesis. To address this, we depleted Neurog2 and NeuroD1 from trigeminal placode cells with morpholinos and demonstrated that Neurog2 and NeuroD1 influence trigeminal ganglion development. While knockdown of both Neurog2 and NeuroD1 affected innervation of the eye, Neurog2 and NeuroD1 had opposite effects on ophthalmic nerve branch organization. Taken together, our results highlight, for the first time, functional roles for Neurog2 and NeuroD1 during chick trigeminal gangliogenesis. These studies shed new light on the molecular mechanisms underlying trigeminal ganglion formation and may also provide insight into general cranial gangliogenesis and diseases of the peripheral nervous system. Full article

(This article belongs to the Special Issue From Cell to Embryo: A Theme Issue Honoring Professor Dr. Roberto Mayor)

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42 pages, 1992 KB

Open AccessFeature PaperEditor’s ChoiceReview

Generation of Lens Progenitor Cells and Lentoid Bodies from Pluripotent Stem Cells: Novel Tools for Human Lens Development and Ocular Disease Etiology

by Aleš Cvekl and Michael John Camerino

Cells 2022, 11(21), 3516; https://doi.org/10.3390/cells11213516 - 6 Nov 2022

Cited by 12 | Viewed by 4944

Abstract

In vitro differentiation of human pluripotent stem cells (hPSCs) into specialized tissues and organs represents a powerful approach to gain insight into those cellular and molecular mechanisms regulating human development. Although normal embryonic eye development is a complex process, generation of ocular organoids and specific ocular tissues from pluripotent stem cells has provided invaluable insights into the formation of lineage-committed progenitor cell populations, signal transduction pathways, and self-organization principles. This review provides a comprehensive summary of recent advances in generation of adenohypophyseal, olfactory, and lens placodes, lens progenitor cells and three-dimensional (3D) primitive lenses, “lentoid bodies”, and “micro-lenses”. These cells are produced alone or “community-grown” with other ocular tissues. Lentoid bodies/micro-lenses generated from human patients carrying mutations in crystallin genes demonstrate proof-of-principle that these cells are suitable for mechanistic studies of cataractogenesis. Taken together, current and emerging advanced in vitro differentiation methods pave the road to understand molecular mechanisms of cataract formation caused by the entire spectrum of mutations in DNA-binding regulatory genes, such as PAX6, SOX2, FOXE3, MAF, PITX3, and HSF4, individual crystallins, and other genes such as BFSP1, BFSP2, EPHA2, GJA3, GJA8, LIM2, MIP, and TDRD7 represented in human cataract patients. Full article

(This article belongs to the Special Issue New Advances in Lens Biology and Pathology)

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17 pages, 1987 KB

Open AccessFeature PaperArticle

Mutations in SIX1 Associated with Branchio-oto-Renal Syndrome (BOR) Differentially Affect Otic Expression of Putative Target Genes

by Tanya Mehdizadeh, Himani D. Majumdar, Sarah Ahsan, Andre L. P. Tavares and Sally A. Moody

J. Dev. Biol. 2021, 9(3), 25; https://doi.org/10.3390/jdb9030025 - 30 Jun 2021

Cited by 11 | Viewed by 4094

Abstract

Several single-nucleotide mutations in SIX1 underlie branchio-otic/branchio-oto-renal (BOR) syndrome, but the clinical literature has not been able to correlate different variants with specific phenotypes. We previously assessed whether variants in either the cofactor binding domain (V17E, R110W) or the DNA binding domain (W122R, Y129C) might differentially affect early embryonic gene expression, and found that each variant had a different combination of effects on neural crest and placode gene expression. Since the otic vesicle gives rise to the inner ear, which is consistently affected in BOR, herein we focused on whether the variants differentially affected the otic expression of genes previously found to be likely Six1 targets. We found that V17E, which does not bind Eya cofactors, was as effective as wild-type Six1 in reducing most otic target genes, whereas R110W, W122R and Y129C, which bind Eya, were significantly less effective. Notably, V17E reduced the otic expression of prdm1, whereas R110W, W122R and Y129C expanded it. Since each mutant has defective transcriptional activity but differs in their ability to interact with Eya cofactors, we propose that altered cofactor interactions at the mutated sites differentially interfere with their ability to drive otic gene expression, and these differences may contribute to patient phenotype variability. Full article

(This article belongs to the Special Issue Craniofacial Genetics and Developmental Biology)

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