Academic literature on the topic 'Otocyst'

Chick embryo otocyst organ cultures were subjected to live vesicular stomatitis virus and rubella virus preparations, to interferon (IFN), and to a combination of both virus and IFN, and compared to control untreated otocysts, We observed morphologic and microscopic changes suggestive of individual cell death and delayed organ differentiation in the virus-treated groups, along with an appreciable decrease in size of the otocyst. Low-dose IFN treatment prior to virus inoculation appeared to partially prevent these effects. The addition of IFN alone did not seem to affect the differentiation process. Time-lapse videophotography further confirmed the above findings. This study suggests that the peripheral component of congenital deafness associated with viral infections is likely to be an effect of the virus itself, and not of the IFN. Interferon provides a partial protective effect against the insult from the virus in vitro and does not seem to be toxic to the developing otocyst.

The otocyst is the epithelial anlage of the membranous labyrinth which interacts with surrounding cephalic mesenchyme to form an otic capsule. A series of in vitro studies was performed to gain a better understanding of the epithelial—mesenchymal interactions involved in this process. Parallel series of otocyst/mesenchyme (O/M) and isolated periotic mesenchyme (M) explants provided morphological and biochemical data to define the role of the otocyst in organizing and directing formation of its cartilaginous otic capsule. Explants were made from mouse embryos ranging in age from 10 to 14 days of gestation, and organ cultured under identical conditions until the chronological equivalent of 16 days of gestation. Expression of chrondrogenesis was determined by both histology and biochemistry. The in vitro behaviour of periotic mesenchyme explanted either with or without an otocyst supports several hypotheses that explain aspects of otic capsule development. The results indicate that (a) prior to embryonic day 12 the otocyst alone is not sufficient to stimulate chondrogenesis of the otic capsule within O/M explants; (b) the otocyst acts as an inductor of capsule chondrogenesis within O/M explants between embryonic days 12 to 13; (c) isolated mesenchyme within M explants taken from 13-day-old embryos are capable of initiating in vitro chondrogenesis, but without expressing capsule morphology in the absence of the otocyst; and (d) the isolated mesenchyme of M explants obtained from 14-day-old embryos expresses both chondrogenesis and otic capsule morphology in the absence of the otocyst. These findings suggest that the otocyst acts as an inductor of chondrogenesis of periotic mesenchyme tissue between embryonic days 11 to 13, and controls capsular morphogenesis between embryonic days 13 to 14 in the mouse embryo.

Fgf3 has long been implicated in otic placode induction and early development of the otocyst; however, the results of experiments in mouse and chick embryos to determine its function have proved to be conflicting. In this study, we determined fgf3 expression in relation to otic development in the zebrafish and used antisense morpholino oligonucleotides to inhibit Fgf3 translation. Successful knockdown of Fgf3 protein was demonstrated and this resulted in a reduction of otocyst size together with reduction in expression of early markers of the otic placode.fgf3 is co-expressed with fgf8 in the hindbrain prior to otic induction and, strikingly, when Fgf3 morpholinos were co-injected together with Fgf8 morpholinos, a significant number of embryos failed to form otocysts. These effects were made manifest at early stages of otic development by an absence of early placode markers (pax2.1 and dlx3) but were not accompanied by effects on cell division or death. The temporal requirement for Fgf signalling was established as being between 60% epiboly and tailbud stages using the Fgf receptor inhibitor SU5402. However, the earliest molecular event in induction of the otic territory, pax8 expression, did not require Fgf signalling, indicating an inductive event upstream of signalling by Fgf3 and Fgf8. We propose that Fgf3 and Fgf8 are required together for formation of the otic placode and act during the earliest stages of its induction.

The expression of nerve growth factor receptors (NGFRs) was studied in the developing inner ear with in situ hybridization in chick embryos and with immunocytochemistry in rat embryos to determine sites of possible functions of NGF or NGF-like molecules in inner ear development. NGFR expression in the chick otocyst and acoustic ganglion is compared with epithelial differentiation and the onset of afferent innervation as determined with fluorescent carbocyanine tracers. In the inner ear of the chick embryo, NGFR mRNA expression shows an alternating pattern in mesenchymal and epithelial tissues. NGFR mRNA is heavily expressed in the mesenchyme surrounding the otocyst (E2-3), ceases at E3-5, and reappears in a thin layer of mesenchymal cells surrounding the membraneous epithelia (E5-13). In the otocyst epithelium, NGFR mRNA expression develops in one anterior and one posterior focus at E3-4.5. NGFR mRNA is expressed in the primordia of the ampullary cristae (E5-7) and possibly the anlage of the utricle; label transiently concentrates in the planum semilunatum of the cristae ampullares and in superior portions of the semicircular canals at E9, but is not seen in differentiating hair cells. In the acoustic ganglion, NGFR mRNA expression begins at E4; at the same time, the first peripheral acoustic nerve processes penetrate the otic epithelium (E4-4.5). The acoustic ganglia remain weakly NGFR mRNA-labeled in the posthatch animal. In the rat embryo, NGFR immunoreactivity is present in the auditory placode at E9, in the periotic mesenchyme at E9-10, and in the medial half of the otocyst at E10-11. At E12, epithelial NGFR expression becomes restricted anteriorly and posteriorly in a pattern similar to that of the chick otocyst and ceases at E13. NGFR immunoreactivity appears transiently in pillar cells of the cochlea in the third week of gestation. NGFR and NGFR mRNA is expressed after E11 in the acoustic ganglia. While NGFR transcripts are expressed in the cochlear ganglion cell bodies, NGFR protein becomes restricted to neuronal processes by the third week of gestation. The vestibular, but not the cochlear (spiral) ganglia remain NGFR-labeled in the adult rat. Onset of NGFR mRNA expression in the acoustic ganglion during the period of afferent fiber ingrowth into the otocyst epithelium is consistent with the hypothesis that NGF-like molecules may have a neurotrophic function for acoustic ganglion cells. Transient expression of NGFRs in secretory cells of the vestibular endorgan and pillar cells in the organ of Corti implicate a role for neurotrophins in the differentiation of these epithelial cell types.

Children with congenital vestibular disorders show delayed motor development and challenges in maintaining posture and balance. Computed tomography images reveal that these children have abnormal inner ears in the form of a sac, with the semicircular canals missing or truncated. Little is known about how this inner ear abnormality affects central vestibular development. At present, mice with the chromodomain helicase DNA-binding protein 7 mutation are the most common model for studying congenital vestibular disorders, despite forming multiple diverse inner ear phenotypes and inducing abnormal cerebellar and visual system development. To identify the effects of a sac-like inner ear on central vestibular development, we have designed and implemented a new model, the anterior-posterior axis rotated otocyst (ARO) chick, which forms a sac-like inner ear in 85% of cases. The ARO chick is produced by anterior-posterior rotation of the otocyst at embryonic day 2. Here, we describe for the first time the 15% of ARO chicks that form three small semicircular canals and rename the ARO chicks forming sacs (ARO/s chicks). The basic features of the vestibular sensory organs in ARO/s chicks are similar to those found in patients’ sacs, and ARO/s hatchlings experience balance and walking problems like patients. Thus, ARO/s chicks have a reproducible inner ear phenotype without abnormalities in vestibular-related structures, making the model a relatively simple one to evaluate the relationship between the sac-like inner ear pathology and formation of the central vestibular neural circuitry. Here, we describe unpublished details on the surgical approaches to produce ARO chicks, including pitfalls and difficulties to avoid. NEW & NOTEWORTHY This paper describes simple techniques for chick otocyst rotation resulting in a sac-like inner ear (85%), the common phenotype in congenital vestibular disorders. We now describe anterior-posterior axis rotated otocyst chicks, which form three small canals (15%), and rename chicks forming a sac (ARO/s chicks). Basic protocols and potential complications of otocyst rotation are described. With the use of ARO/s chicks, it will be possible to determine how the vestibular neural circuit is modified by sac-like inner ear formation.

Objectives: We sought to determine the developmental anatomy and EYA1 protein distribution in the inner ear of Xenopus laevis. Methods: Xenopus laevis embryos were stained with monoclonal antibodies and imaged with confocal microscopy. Results: At stage 27, the otocyst fully forms, with strong tubulin staining of early sensory cells at its ventromedial aspect. Neuronal ingrowth follows at stage 33/34. At stage 50, the semicircular canals are complete. EYA1 localizes to the anterior aspect of the otocyst from stages 37 to 44. By stage 50, EYA1 distribution is localized primarily to the sensory maculae and the endolymphatic duct of the developing inner ear. Conclusions: Whole mount confocal imaging of the developing Xenopus inner ear delineates the exact timing of otic development, sensory cell differentiation, and innervation. EYA1 protein expression has a distinct distribution pattern at the anterior aspect of the developing otocyst in stages 41 and 44. Later stages have a more localized pattern, in which EYA1 is detected only in the sensory epithelium and endolymphatic duct. This specific pattern of expression indicates a possible role in the determination of the anterior-posterior orientation of the inner ear, as well as a later role in sensory cell differentiation.

Development of the vertebrate inner ear is characterized by a series of genetically programmed events involving induction of surface ectoderm, preliminary morphogenesis, specification and commitment of sensory, nonsensory and neuronal cells, as well as outgrowth and restructuring of the otocyst to form a complex labyrinth. Hmx2, a member of the Hmx homeobox gene family, is coexpressed with Hmx3 in the dorsolateral otic epithelium. Targeted disruption of Hmx2 in mice demonstrates the temporal and spatial involvement of Hmx2 in the embryonic transition of the dorsal portion (pars superior) of the otocyst to a fully developed vestibular system. In Hmx2 null embryos, a perturbation in cell fate determination in the lateral aspect of the otic epithelium results in reduced cell proliferation in epithelial cells, which includes the vestibular sensory patches and semicircular duct fusion plates, as well as in the adjacent mesenchyme. Consequently, enlargement and morphogenesis of the pars superior of the otocyst to form a complex labyrinth of cavities and ducts is blocked, as indicated by the lack of any distinguishable semicircular ducts, persistence of the primordial vestibular diverticula, significant loss in the three cristae and the macula utriculus, and a fused utriculosaccular chamber. The developmental regulators Bmp4, Dlx5 and Pax2 all play a critical role in inner ear ontogeny, and the expression of each of these genes is affected in the Hmx2 null otocyst suggesting a complex regulatory role for Hmx2 in this genetic cascade. Both Hmx2 and Hmx3 transcripts are coexpressed in the developing central nervous system including the neural tube and hypothalamus. A lack of defects in the CNS, coupled with the fact that not all of the Hmx2-positive regions in developing inner ear are impaired in the Hmx2 null mice, suggest that Hmx2 and Hmx3 have both unique and overlapping functions during embryogenesis.

Mammalian monogamy is puzzling from and evolutionary perspective because it is unclear why males, which have the potential to father a great many offspring, should choose to associate with only one female. This project investigated the behaviour of a socially monogamous (pair-living) population of bat-eared foxes in Laikipia, Northern Kenya, and had two principal aims. The first aim was to identify the selective forces that operate to maintain social monogamy in the study population. The second aim was to determine whether bat-eared foxes mate exclusively with their social partners (i. e. if they are genetically as well as socially monogamous). Chapter I summarizes by background to the research: Broadly speaking, theories advanced to explain the evolution of monogamy fall into two categories; those that proposing that monogamy occurs when male assistance is required for successfW reproduction, and those that proposing that aspects of female spatial and/or temporal distribution make it impossible for even the most competitive males to gain more than one mate. Chapter 2 describes the study site and general methods employed. Chapter 3 examines whether a requirement for paternal care maintains social monogamy by investigating the parental roles of males and females: I found that females invest very heavily in reproduction, feeding at close to maximum rate throughout lactation and suffering increased mortality rates during this period. Consistent with previous studies of the species, I found that males are heavily involved in the rearing of young, spending significantly more time than females close to breeding dens, and contributing to all aspects of cub care. The importance of male care was revealed by the fact that, after statistically controlling for the confounding effects of territory quality, the male den attendance was significantly associated with cub survival. Chapter 4 investigates factors other than the requirement for male care that may prevent males from achieving polygynous status: Social monogamy was not enforced because males were incapable of defending sufficient resources to support more than one female, as some male territories contained sufficient food to support two or more females. I found, however, that because females occupied largely exclusive ranges and had synchronized fertile periods, it was probably impossible for even the most competitive males to successfully defend more than one fertile female. Chapter 5 investigates the mating tactics of bat-eared foxes by comparing their behaviour during and outside the mating season: Neither male nor female foxes increased their home range sizes during the mating season, demonstrating that they do not roam widely in search of extra-pair mates. Time-budget data suggest that this may be because bat-eared foxes have little time available to engage in activities other than foraging. The behaviour of mated partners wass highly coordinated, particularly during the mating season, and the close proximity of mated partners did not reduce their feeding rate. Chapter 6 uses DNA microsatellite analyses to establish the paternity of bat-eared fox cubs: We found that for the vast majority of cubs (42 of 44) social fathers were most likely to be their true fathers. These data demonstrate a high level of genetic monogamy in the study population. Chapter 7 summarizes data from the thesis: I conclude that, although male care enhances offspring survival, there are circumstances under which males may gain from polygyny. Males are probably unable to attain polygynous status, however, because the spatial and temporal distribution of females, combined with intense competition for mates makes it impossible for them to defend more than one mate. Consistent with observations of occasional polygynous breeding from other bat-eared fox populations, I conclude that polygyny could only a viable male strategy if compliant females were willing to co-ordinated their behaviour. I argue that the high levels of genetic monogamy observed are probably consequence of the species insectivorous diet, which leaves individuals with little time to engage in activities other than foraging, and makes it easy for males to guard their own partners.

Loss of hearing affects more than 10 % of the population, and one newborn in a thousand is born with defects of the inner ear. Transcriptional factors involved in the development of inner ear are important in our understanding of the causes of inner ear defects. ISLET1 is one of these factors. ISLET1 expression is detected in the sensory and neuronal cells of the inner ear. It participates in otocyst formation, and the specification and differentiation of cells of cochlea and vestibular system. The functional role of ISLET1 during inner ear development was investigated. Its role was studied by using Pax2-Isl1 transgenic mice that overexpress Islet1 under the control of the Pax2 promoter. Two transgenic lines were generated, Pax2-Isl1/300 and Pax2- Isl1/52. Two copies of the Pax2-Isl1 transgene were inserted to Pax2-Isl1/300 genome and one copy was inserted to the Pax2-Isl1/52 genome. Defects in sense of hearing were detected in both lines and circling behavior, a defect of balance, was detected in the Pax2-Isl1/300 transgenic mice. We observed high postnatal lethality in heterozygote transgenic mice. Pax2-Isl1/52 homozygote mutation is lethal at embryonic day 10 (E10,5). Pax2-Isl1/300 homozygote letality couldn't be detected because of the inability to breed heterozygote mutated mice of this line....