Neural crest and the patterning of vertebrate craniofacial muscles.

Patterning of craniofacial muscles overtly begins with the activation of lineage-specific markers at precise, evolutionarily conserved locations within prechordal, lateral, and both unsegmented and somitic paraxial mesoderm populations. Although these initial programming events occur without influence of neural crest cells, the subsequent movements and differentiation stages of most head muscles are neural crest-dependent. Incorporating both descriptive and experimental studies, this review examines each stage of myogenesis up through the formation of attachments to their skeletal partners.

Deep sequencing of the uterine immune response to bacteria during the equine oestrous cycle.

Background: The steroid hormone environment in healthy horses seems to have a significant impact on the efficiency of their uterine immune response. The objective of this study was to characterize the changes in gene expression in the equine endometrium in response to the introduction of bacterial pathogens and the influence of steroid hormone concentrations on this expression.

Methods: Endometrial biopsies were collected from five horses before and 3 h after the inoculation of Escherichia coli once in oestrus (follicle >35 mm in diameter) and once in dioestrus (5 days after ovulation) and analysed using high-throughput RNA sequencing techniques (RNA-Seq).

Effect of ovarian hormones on the healthy equine uterus: a global gene expression analysis.

The physiological changes associated with the varying hormonal environment throughout the oestrous cycle are linked to the different functions the uterus needs to fulfil. The aim of the present study was to generate global gene expression profiles for the equine uterus during oestrus and Day 5 of dioestrus. To achieve this, samples were collected from five horses during oestrus (follicle >35 mm in diameter) and dioestrus (5 days after ovulation) and analysed using high-throughput RNA sequencing techniques (RNA-Seq).

A new heart for a new head in vertebrate cardiopharyngeal evolution.

It has been more than 30 years since the publication of the new head hypothesis, which proposed that the vertebrate head is an evolutionary novelty resulting from the emergence of neural crest and cranial placodes. Neural crest generates the skull and associated connective tissues, whereas placodes produce sensory organs. However, neither crest nor placodes produce head muscles, which are a crucial component of the complex vertebrate head.

The left-right Pitx2 pathway drives organ-specific arterial and lymphatic development in the intestine.

The dorsal mesentery (DM) is the major conduit for blood and lymphatic vessels in the gut. The mechanisms underlying their morphogenesis are challenging to study and remain unknown. Here we show that arteriogenesis in the DM begins during gut rotation and proceeds strictly on the left side, dependent on the Pitx2 target gene Cxcl12.

Imaging diagnosis--meningoencephalitis secondary to suppurative rhinitis and meningoencephalocele infection in a dog.

Nasal encephaloceles (meningoceles or meningoencephaloceles) are rare and not reported to be infected or coupled with a facial deformity in dogs. This report describes an older dog with acute worsening of seizures due to suppurative meningoencephalitis with coexisting suppurative rhinitis and infection of a meningoencephalocele. Additionally, the dog had a facial deformity for at least 5 years.

Disease severity in a mouse model of ataxia telangiectasia is modulated by the DNA damage checkpoint gene Hus1.

The human genomic instability syndrome ataxia telangiectasia (A-T), caused by mutations in the gene encoding the DNA damage checkpoint kinase ATM, is characterized by multisystem defects including neurodegeneration, immunodeficiency and increased cancer predisposition. ATM is central to a pathway that responds to double-strand DNA breaks, whereas the related kinase ATR leads a parallel signaling cascade that is activated by replication stress. To dissect the physiological relationship between the ATM and ATR pathways, we generated mice defective for both.

Intrinsic properties guide proximal abducens and oculomotor nerve outgrowth in avian embryos.

Proper movement of the vertebrate eye requires the formation of precisely patterned axonal connections linking cranial somatic motoneurons, located at defined positions in the ventral midbrain and hindbrain, with extraocular muscles. The aim of this research was to assess the relative contributions of intrinsic, population-specific properties and extrinsic, outgrowth site-specific cues during the early stages of abducens and oculomotor nerve development in avian embryos. This was accomplished by surgically transposing midbrain and caudal hindbrain segments, which had been pre-labeled by electroporation with an EGFP construct.

Shmt1 and de novo thymidylate biosynthesis underlie folate-responsive neural tube defects in mice.

Background: Folic acid supplementation prevents the occurrence and recurrence of neural tube defects (NTDs), but the causal metabolic pathways underlying folic acid-responsive NTDs have not been established. Serine hydroxymethyltransferase (SHMT1) partitions folate-derived one-carbon units to thymidylate biosynthesis at the expense of cellular methylation, and therefore SHMT1-deficient mice are a model to investigate the metabolic origin of folate-associated pathologies.

Objectives: We examined whether genetic disruption of the Shmt1 gene in mice induces NTDs in response to maternal folate and choline deficiency and whether a corresponding disruption in de novo thymidylate biosynthesis underlies NTD pathogenesis.

Mouse H6 Homeobox 1 (Hmx1) mutations cause cranial abnormalities and reduced body mass.

Background: The H6 homeobox genes Hmx1, Hmx2, and Hmx3 (also known as Nkx5-3; Nkx5-2 and Nkx5-1, respectively), compose a family within the NKL subclass of the ANTP class of homeobox genes. Hmx gene family expression is mostly limited to sensory organs, branchial (pharyngeal) arches, and the rostral part of the central nervous system. Targeted mutation of either Hmx2 or Hmx3 in mice disrupts the vestibular system.

Neural crest cells and the community of plan for craniofacial development: historical debates and current perspectives.

After their initial discovery in the mid 1800s, neural crest cells transitioned from the category of renegade intra-embryonic wanderers to achieve rebel status, provoked especially by the outrageous claim that they participate in skeletogenesis, an embryonic event theretofore reserved exclusively for mesoderm. Much of the 20th century found neural crest cells increasingly viewed as a unique population set apart from other embryonic populations and more often treated as orphans rather than fully embraced by mainstream developmental biology. Now frequently touted as a fourth germ layer, the neural crest has become a fundamental character for distinguishing craniates from other metazoans, and has radically redefined perceptions about the organization and evolution of the vertebrate jaws and head.

The differentiation and morphogenesis of craniofacial muscles.

Unraveling the complex tissue interactions necessary to generate the structural and functional diversity present among craniofacial muscles is challenging. These muscles initiate their development within a mesenchymal population bounded by the brain, pharyngeal endoderm, surface ectoderm, and neural crest cells. This set of spatial relations, and in particular the segmental properties of these adjacent tissues, are unique to the head.

Spatial relations between avian craniofacial neural crest and paraxial mesoderm cells.

Fate maps based on quail-chick grafting of avian cephalic neural crest precursors and paraxial mesoderm cells have identified the majority of derivatives from each population but have not unequivocally resolved the precise locations of and population dynamics at the interface between them. The relation between these two mesenchymal tissues is especially critical for the development of skeletal muscles, because crest cells play an essential role in their differentiation and subsequent spatial organization. It is not known whether myogenic mesoderm and skeletogenic neural crest cells establish permanent relations while en route to their final destinations, or later at the sites where musculoskeletal morphogenesis is completed.

Relations and interactions between cranial mesoderm and neural crest populations.

The embryonic head is populated by two robust mesenchymal populations, paraxial mesoderm and neural crest cells. Although the developmental histories of each are distinct and separate, they quickly establish intimate relations that are variably important for the histogenesis and morphogenesis of musculoskeletal components of the calvaria, midface and branchial regions. This review will focus first on the genesis and organization within nascent mesodermal and crest populations, emphasizing interactions that probably initiate or augment the establishment of lineages within each.

Normal and aberrant craniofacial myogenesis by grafted trunk somitic and segmental plate mesoderm.

Our research assesses the ability of three trunk mesodermal populations -- medial and lateral halves of newly formed somites, and presomitic (segmental plate) mesenchyme -- to participate in the differentiation and morphogenesis of craniofacial muscles. Grafts from quail donor embryos were placed in mesodermal pockets adjacent to the midbrain-hindbrain boundary, prior to the onset of neural crest migration, in chick host embryos. This encompasses the site where the lateral rectus and the proximal first branchial arch muscle primordia arise.

Appearance of neurons and glia with respect to the wavefront during colonization of the avian gut by neural crest cells.

The enteric nervous system is formed by neural crest cells that migrate, proliferate, and differentiate into neurons and glia distributed in ganglia along the gastrointestinal tract. In the developing embryo some enteric crest cells cease their caudal movements, whereas others continue to migrate. Subsequently, the enteric neurons form a reticular network of ganglia interconnected by axonal projections.