scholarly journals The Fgf8 subfamily (Fgf8, Fgf17 and Fgf18) is required for closure of the embryonic ventral body wall

Development ◽  
2020 ◽  
Vol 147 (21) ◽  
pp. dev189506 ◽  
Author(s):  
Michael Boylan ◽  
Matthew J. Anderson ◽  
David M. Ornitz ◽  
Mark Lewandoski
Keyword(s):  
Birth Defect ◽  
Body Wall ◽  
Abdominal Muscles ◽  
Fibroblast Growth ◽  
Internal Organs ◽  
Mouse Mutants ◽  
Major Class ◽  
Morphogenetic Event ◽  
Ventral Wall ◽  
Significant Health

ABSTRACTThe closure of the embryonic ventral body wall in amniotes is an important morphogenetic event and is essential for life. Defects in human ventral wall closure are a major class of birth defect and a significant health burden. Despite this, very little is understood about how the ventral body wall is formed. Here, we show that fibroblast growth factor (FGF) ligands FGF8, FGF17 and FGF18 are essential for this process. Conditional mouse mutants for these genes display subtle migratory defects in the abdominal muscles of the ventral body wall and an enlarged umbilical ring, through which the internal organs are extruded. By refining where and when these genes are required using different Cre lines, we show that Fgf8 and Fgf17 are required in the presomitic mesoderm, whereas Fgf18 is required in the somites. This study identifies complex and multifactorial origins of ventral wall defects and has important implications for understanding their origins during embryonic development.

The Imaginal Ecdysis of Blowflies. The Control of Cuticuar Hardening and Darkening

1962 ◽  
Vol 39 (3) ◽  
pp. 395-412
Author(s):  
C. B. COTTRELL
Keyword(s):  
Blood Transfusion ◽  
Critical Period ◽  
Body Wall ◽  
The Body ◽  
Internal Organs ◽  
Active Factor

1. Blood transfusion experiments show that normal hardening and darkening at the imaginal ecdysis of CaUiphora erythrocephala (Meigen) is brought about by the release into the blood of an active factor. Introduction of this factor into a newly emerged fly some 35 min. prior to the time at which it would normally be released is sufficient to prevent expansion. 2. The factor is normally released some 45 min. before the appearance of the first signs of darkening and between 3 and 15 min. after the fly has reached conditions suitable for expansion, that is at about the time of initiation of air-pumping. 3. Decapitation at emergence will prevent the initiation of normal hardening and darkening but not of secondary darkening. Evidently the head is concerned in the release or the control of the release of the blood-borne darkening factor. 4. The critical period for the prevention of normal hardening and darkening by decapitation lies between 3 and 15 min. after the fly has reached conditions suitable for expansion. 5. Isolated abdomina behave in a manner similar to decapitated flies but their reactions are complicated by secondary darkening associated with damage. 6. Flies deprived of their abdomina will expand at least partially but the rate of their hardening and darkening is reduced. 7. Damage reactions resembling secondary darkening in digging flies are more extensive after damage to internal organs such as the gut than to superficial organs such as the body wall. 8. Allowing for the effects of secondary darkening it is possible to demonstrate the occurrence of the blood-borne darkening factor by means of ligatures placed at emergence between the thorax and the abdomen. Under these conditions only the head and thorax exhibit normal darkening.

scholarly journals Thanatophoric Skeletal Dysplasia: A Case Report

2020 ◽  
Vol 58 (223) ◽  
pp. 185-187
Author(s):  
Firoz Anjum ◽  
Sunil Kumar Daha ◽  
Ganesh Sah
Keyword(s):  
Skeletal Dysplasia ◽  
Birth Defect ◽  
Fibroblast Growth Factor Receptor ◽  
Similar Case ◽  
De Novo ◽  
Growth Factor Receptor ◽  
De Novo Mutation ◽  
Fibroblast Growth ◽  
Vertebral Bodies ◽  
Almost All

Thanatophoric skeletal dysplasia is the most lethal, rare, sporadic birth defect due to de novo mutation in the fibroblast growth factor receptor-3. Clinically this is characterized by shortening of the limbs (micromelia), small conical thorax, flat vertebral bodies and macrocephaly at birth. We encountered a similar case with ultrasonographic findings suggestive of Thanatophoric skeletal dysplasia which resulted into death of the baby within an hour of birth. Almost all cases of this condition have been reported to have died interuterinally or few days after birth.

On certain Semi-carnivorous Anthomyid Larvae

Parasitology ◽  
1930 ◽  
Vol 22 (2) ◽  
pp. 168-181 ◽  
Author(s):  
D. Keilin ◽  
P. Tate
Keyword(s):  
Alimentary Canal ◽  
Body Wall ◽  
Anatomical Structure ◽  
The Body ◽  
Sensory Organs ◽  
Ventral Region ◽  
Anatomical Features ◽  
Mode Of Life ◽  
Ventral Wall

In previous papers one of us (Keilin, 1915, 1917) has shown that among cyclorrhaphous dipterous larvae there is a remarkable correlation between the anatomical structure of the larvae and their mode of life. Although the mode of life of the larvae is in correlation with such anatomical features as thickness and hardness of the body-wall, the development of sensory organs on the head, and the structure of the alimentary canal, it is in the bucco-pharyngeal armature that the most obvious and important adaptations are to be found. The most important of these adaptations may be mentioned briefly. In certain cyclorrhaphous dipterous larvae the ventral wall of the basal sclerite of the bucco-pharyngeal armature has a number of longitudinal ridges projecting into the lumen of the pharynx. These ridges are usually Y-shaped at their free borders, and form a series of longitudinal channels in the ventral region of the pharynx. In other cyclorrhaphous dipterous larvae such ridges are absent and the ventral wall of the pharynx is smooth. This character allows the larvae to be divided into two groups—“all cyclorrhaphous dipterous larvae parasitic on the most diverse animals or on plants, as well as carnivorous larvae, and larvae which suck the blood of mammals, never have ridges in their pharynx; on the contrary, ridges are always present in saprophagous larvae” (Keilin, 1915). All the larvae which are devoid of ridges and are either parasitic, carnivorous, pass their whole life in the uterus of the female, or are phytophagous, may be united into the group of biontophagous; all larvae which have ridges are saprophagous.

The Larval and Pupal Anatomy of Stenomalus micans Ol. (Pteromalidae), a Chalcid Endoparasite of the Gout-fly of Barley (Chlorops taeniopus Meig.), with some Details of the Life History of the Summer Generation

Parasitology ◽  
1931 ◽  
Vol 23 (3) ◽  
pp. 380-395 ◽  
Author(s):  
H. G. H. Kearns
Keyword(s):  
Body Wall ◽  
Saline Solution ◽  
Larval Instar ◽  
Physiological Saline ◽  
Instar Larva ◽  
Fourth Instar Larva ◽  
Internal Organs ◽  
Tracheal System ◽  
Physiological Saline Solution ◽  
History Of

1. Two species of endoparasites, a Chalcid Stenomalus micans and a Braconid Coelineus niger, were found in every sample of “gouted” barley examined from a number of counties in southern England.2. Chlorops infestations were severe in 1928 in many districts, and the majority of the “gouted” shoots were of winter-type damage, of which 68 percent. were parasitised, two-thirds by S. micans.3. The larval anatomy of S. micans is described:(a) There are five larval instars, each of which is described.(b) The first larval instar appears to be partly predaceous.(c) The larvae can be kept alive for 5 days on the surface of normal physiological saline solution and moulting occurs, which enables the instar to be determined with certainty.(d) The tracheal system is devoid of spiracles until the fourth larval instar; spiracles then develop and are connected to the former rudimentary stigmatic trunks prior to the death of the host.(e) The fourth instar larva develops a cephalic boring armature which is used for breaking up the internal organs of the host and also to bore an exit hole through the latter's body wall.4. The pupa of S. micans is described and sex differences are indicated.

scholarly journals Fibroblast Growth Factor Signalling in the Diseased Nervous System

2021 ◽  
Author(s):  
Lars Klimaschewski ◽  
Peter Claus
Keyword(s):  
Nervous System ◽  
Imaging Techniques ◽  
Fibroblast Growth ◽  
Maintenance And Repair ◽  
Signalling Molecules ◽  
Mouse Mutants ◽  
Tissue Protection ◽  
Growth Factor Signalling ◽  
Fgf Signalling

AbstractFibroblast growth factors (FGFs) act as key signalling molecules in brain development, maintenance, and repair. They influence the intricate relationship between myelinating cells and axons as well as the association of astrocytic and microglial processes with neuronal perikarya and synapses. Advances in molecular genetics and imaging techniques have allowed novel insights into FGF signalling in recent years. Conditional mouse mutants have revealed the functional significance of neuronal and glial FGF receptors, not only in tissue protection, axon regeneration, and glial proliferation but also in instant behavioural changes. This review provides a summary of recent findings regarding the role of FGFs and their receptors in the nervous system and in the pathogenesis of major neurological and psychiatric disorders.

Myoblast migration specifically inhibited in the chick embryo by grafted CSAT hybridoma cells secreting an anti-integrin antibody

Development ◽  
1988 ◽  
Vol 103 (3) ◽  
pp. 431-446 ◽  
Author(s):  
T. Jaffredo ◽  
A.F. Horwitz ◽  
C.A. Buck ◽  
P.M. Rong ◽  
F. Dieterlen-Lievre
Keyword(s):  
Chick Embryo ◽  
Body Wall ◽  
Developmental Process ◽  
Hybridoma Cells ◽  
General Interest ◽  
Abdominal Muscles ◽  
Muscle Formation ◽  
Body Wall Muscles ◽  
Long Term Consequences

We report a teratological method in which mouse hybridoma cells are grafted into a chick host. CSAT (Cell Substratum ATtachment) hybridoma was used. It produces an antibody directed against the avian integrin complex. The grafts were performed during the second and third days of incubation either at the level of the somites or in the coelom of the chick embryo. The anomalies were revealed by means of a monoclonal antibody that recognizes myogenic cells as soon as they become committed in the myotome. When embryos were grafted at the level of the somites, body wall muscles failed to develop on the side of the graft only. After coelomic grafting, total agenesis of abdominal muscles was induced. The anomalies were specific since the engraftment of three control hybridoma clones induced no change in muscle formation. These control hybridomas produce antibodies directed against the same molecular complex but not against the same epitope as CSAT. The injection of hybridoma cells in an embryo appears as a method of general interest to determine the long-term consequences of perturbing a specific developmental process.

The abdominal muscles, and the mechanical displacement of the internal organs.

2011 ◽  
pp. 117-122
Author(s):  
W. F. Evans
Keyword(s):  
Abdominal Muscles ◽  
Internal Organs ◽  
Mechanical Displacement

Differences in the responses between tissues of the body wall and the internal organs of Phascolosoma arcuatum (Sipuncula) to changes in salinity

1994 ◽  
Vol 107 (1) ◽  
pp. 141-147 ◽  
Author(s):  
Shit F. Chew ◽  
Kah W. Peng ◽  
W.P. Low ◽  
Yuen K. Ip
Keyword(s):  
Body Wall ◽  
The Body ◽  
Internal Organs

scholarly journals Disruption of a hedgehog-foxf1-rspo2 signaling axis leads to tracheomalacia and a loss of sox9+ tracheal chondrocytes

2020 ◽  
pp. dmm.046573
Author(s):  
Talia Nasr ◽  
Andrea M. Holderbaum ◽  
Praneet Chaturvedi ◽  
Kunal Agarwal ◽  
Jessica L. Kinney ◽  
...  
Keyword(s):  
Birth Defect ◽  
Molecular Mechanisms ◽  
Lineage Tracing ◽  
Dramatic Reduction ◽  
Tracheal Cartilage ◽  
Cartilage Development ◽  
Mouse Mutants ◽  
Gli Transcription Factors ◽  
Signaling Axis ◽  
Repressor Activity

Congenital tracheomalacia, resulting from incomplete tracheal cartilage development, is a relatively common birth defect that severely impairs breathing in neonates. Mutations in the Hedgehog (HH) pathway and downstream Gli transcription factors are associated with tracheomalacia in patients and mouse models; however, the underlying molecular mechanisms are unclear. Using multiple HH/Gli mouse mutants including one that mimics Pallister-Hall Syndrome, we show that excessive Gli repressor activity prevents specification of tracheal chondrocytes. Lineage tracing experiments show that Sox9+ chondrocytes arise from HH-responsive splanchnic mesoderm in the fetal foregut that expresses the transcription factor Foxf1. Disrupted HH/Gli signaling results in 1) loss of Foxf1 which in turn is required to support Sox9+ chondrocyte progenitors and 2) a dramatic reduction in Rspo2, a secreted ligand that potentiates Wnt signaling known to be required for chondrogenesis. These results reveal a HH-Foxf1-Rspo2 signaling axis that governs tracheal cartilage development and informs the etiology of tracheomalacia.

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