scholarly journals Size control of the inner ear via hydraulic feedback

2018 ◽  
Author(s):  
Kishore R. Mosaliganti ◽  
Ian A. Swinburne ◽  
Chon U Chan ◽  
Nikolaus D. Obholzer ◽  
Amelia A. Green ◽  
...  
Keyword(s):  
Hydrostatic Pressure ◽  
Inner Ear ◽  
Fluid Transport ◽  
Quantitative Imaging ◽  
Size Variation ◽  
Size Control ◽  
Otic Vesicle ◽  
Physiological Measurement ◽  
Cellular Processes ◽  
Pressure Driven

SUMMARYAnimals make organs of precise size, shape, and symmetry despite noise in underlying molecular and cellular processes. How developing organs manage this noise is largely unknown. Here, we combine quantitative imaging, physical theory, and physiological measurement of hydrostatic pressure and fluid transport in zebrafish to study size control of the developing inner ear. We find that fluid accumulation creates hydrostatic pressure in the lumen leading to stress in the epithelium and expansion of the otic vesicle. Pressure, in turn, inhibits fluid transport into the lumen. This negative feedback loop between pressure and transport allows the otic vesicle to change growth rate to control natural or experimentally-induced size variation. Spatiotemporal patterning of contractility modulates pressure-driven strain for regional tissue thinning. Our work connects moleculardriven mechanisms, such as osmotic pressure driven strain and actomyosin tension, to the regulation of tissue morphogenesis via hydraulic feedback to ensure robust control of organ size.

scholarly journals Size control of the inner ear via hydraulic feedback

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Kishore R Mosaliganti ◽  
Ian A Swinburne ◽  
Chon U Chan ◽  
Nikolaus D Obholzer ◽  
Amelia A Green ◽  
...  
Keyword(s):  
Hydrostatic Pressure ◽  
Inner Ear ◽  
Fluid Transport ◽  
Quantitative Imaging ◽  
Size Variation ◽  
Size Control ◽  
Editorial Note ◽  
Otic Vesicle ◽  
Physiological Measurement ◽  
Pressure Driven

Animals make organs of precise size, shape, and symmetry but how developing embryos do this is largely unknown. Here, we combine quantitative imaging, physical theory, and physiological measurement of hydrostatic pressure and fluid transport in zebrafish to study size control of the developing inner ear. We find that fluid accumulation creates hydrostatic pressure in the lumen leading to stress in the epithelium and expansion of the otic vesicle. Pressure, in turn, inhibits fluid transport into the lumen. This negative feedback loop between pressure and transport allows the otic vesicle to change growth rate to control natural or experimentally-induced size variation. Spatiotemporal patterning of contractility modulates pressure-driven strain for regional tissue thinning. Our work connects molecular-driven mechanisms, such as osmotic pressure driven strain and actomyosin tension, to the regulation of tissue morphogenesis via hydraulic feedback to ensure robust control of organ size.Editorial note: This article has been through an editorial process in which the authors decide how to respond to the issues raised during peer review. The Reviewing Editor's assessment is that all the issues have been addressed (<xref ref-type="decision-letter" rid="SA1">see decision letter</xref>).

The abnormalities of the inner ear in kreisler mice

Development ◽  
1964 ◽  
Vol 12 (3) ◽  
pp. 475-490
Author(s):  
M. S. Deol
Keyword(s):  
Inner Ear ◽  
Recessive Gene ◽  
Cresyl Violet ◽  
Otic Vesicle ◽  
Litter Mate ◽  
Abnormal Position ◽  
Sectioned Material

The recessive gene kreisler (symbol kr) was discovered by Hertwig (1942a), who later described its effects on behaviour (1942b) and the inner ear (1944, 1956). She found that it was possible to trace the anomalies of the ear back to 9-day embryos, when the otic vesicle can be seen to be situated in an abnormal position. The present study was aimed at discovering the cause of this abnormality, and at giving a fuller account of the later development of the ear. Material and Methods The particulars of the sectioned material are given in Table 1. Only litter-mate controls were used throughout. The embryos were fixed in Bouin's fluid, sectioned at 7½ or 10 μ, depending on their age, and stained with Ehrlich's haematoxylin and eosin. The older material was fixed in Witmaack's fluid or formalin, sectioned at 10 μ, and stained either the same way or with cresyl violet or Weil's iron haematoxylin.

Retinoic acid modulation of the early development of the inner ear is associated with the control of c-fos expression

Development ◽  
1990 ◽  
Vol 110 (4) ◽  
pp. 1081-1090 ◽  
Author(s):  
J. Represa ◽  
A. Sanchez ◽  
C. Miner ◽  
J. Lewis ◽  
F. Giraldez
Keyword(s):  
Cell Proliferation ◽  
Retinoic Acid ◽  
Inner Ear ◽  
Early Development ◽  
Otic Vesicle ◽  
Low Concentrations ◽  
Full Effect ◽  
20 Nm ◽  
Otic Vesicles

The effects of retinoic acid (RA) on the early development of the inner ear were studied in vitro using isolated chick embryo vesicles. Low concentrations of RA (1–50 nM) inhibited vesicular growth in stage 18 otic vesicles that were made quiescent and then reactivated by either serum or bombesin. Growth inhibition was concentration-dependent and was paralleled by a reduction in the rate of DNA synthesis as measured by [3H]thymidine incorporation. Half-inhibition occurred between 1 and 10 nM RA, and the full effect at 20 nM. Retinoic acid, in the presence of serum, induced the precocious differentiation of (1) secretory epithelium, the tegmentum vasculosum and endolymphatic sac and (2) early sensory and supporting epithelia. These structures were positioned in their corresponding normal presumptive areas. The overall direction of growth was reversed by RA and the ratio of the internal to the external vesicular surface area increased with RA concentration. The expression of the nuclear proto-oncogene c-fos in the developing otic vesicle was transient and stage-dependent. High levels of c-fos mRNA were positively correlated with cell proliferation. Incubation of growth-arrested otic vesicles with bombesin plus insulin at concentrations that induced cell proliferation produced a strong induction of c-fos. This mitogen-induced expression was suppressed by 25 nM RA. The results suggest (1) a role for retinoic acid in controlling the early development of the inner ear and (2) that this control is effected through the regulation of the proto-oncogene c-fos.

Polarization and density of Na-pumps in the inner ear of the chick embryo during early stages of development

Development ◽  
1987 ◽  
Vol 100 (2) ◽  
pp. 271-278
Author(s):  
F. Giraldez ◽  
J.J. Represa ◽  
L. Borondo ◽  
E. Barbosa
Keyword(s):  
Binding Sites ◽  
Fluid Transport ◽  
Developmental Stages ◽  
Otic Vesicle ◽  
Transient Stage ◽  
Highly Sensitive ◽  
Proliferative Growth ◽  
K Concentration ◽  
Otic Vesicles ◽  
Vectorial Transport

The otic vesicle consists of a pseudostratified epithelium with some features of transporting epithelia. The present work questions whether Na-pumps are polarized in this epithelium and what is the relation between the location or density of pumps and development. This was done by measuring the binding of [3H]ouabain to isolated otic vesicles in developmental stages 16 to 22. The results show the presence of specific ouabain-binding sites located in the inward-facing membrane of the otic vesicle epithelium. Binding was saturable at increasing concentrations of ouabain and was highly sensitive to the external K+ concentration with half-maximal inhibition below 0.5 mM, indicating that the binding sites and Na-pump sites are identical. A transient stage-dependent increase in the density of Na-pumps during the period that precedes growth was observed. Evidence is given against this being directly related to an increased net fluid transport rate despite the fact that pump sites were always polarized throughout these stages. The conclusions are that (1) the otic vesicle epithelium is a polarized structure with the possibility of vectorial transport of solutes and water and (2) the increased number of pumps may operate as a regulatory mechanism during normal proliferative growth.

Pattern of expression of the jun family of transcription factors during the early development of the inner ear: implications in apoptosis

1999 ◽  
Vol 112 (22) ◽  
pp. 3967-3974
Author(s):  
C. Sanz ◽  
Y. Leon ◽  
S. Canon ◽  
L. Alvarez ◽  
F. Giraldez ◽  
...  
Keyword(s):  
Cell Death ◽  
Transcription Factors ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Inner Ear ◽  
Otic Vesicle ◽  
Mobility Shift ◽  
Nerve Growth ◽  
Vestibular Ganglion ◽  
Amino Terminal

Jun transcription factors have been implicated in the regulation of cell proliferation, differentiation and apoptosis. We have investigated the relationship between Jun expression and cell death in the developing chicken inner ear. c-jun and junD transcripts were expressed in the epithelium of the otic placode and otic vesicle. c-jun expression was restricted to the dorsal area of the otic pit (stages 14–17), dorsal otic vesicle and cochleo-vestibular ganglion (stages 18–20). junD expression was transient and occurred in the dorsal and upper medial aspects of the otic pit and otic cup, but it was down-regulated in the otic vesicle. A parallel TUNEL analysis revealed that expression of c-jun co-located within areas of intense apoptosis. Furthermore, phosphorylation of c-Jun at serine-63 by Jun amino-terminal-kinases was detected in the dorsal otic pit, otic vesicle and cochleo-vestibular ganglion. c-Jun protein exhibited DNA binding activity, as assessed by gel mobility shift assays. The association between c-Jun and apoptosis was further demonstrated by studying nerve growth factor-induced apoptosis in cultured otic vesicles. Nerve growth factor-induced cell death and c-Jun phosphorylation that were suppressed by insulin-like growth factor-I and by viral-mediated overexpression of Raf, which had survival effects. In conclusion, the precise regulation of the expression and activity of Jun proteins in the otic primordium suggests that it may operate as a fundamental mechanism during organogenesis.

Nkx5-1 controls semicircular canal formation in the mouse inner ear

Development ◽  
1998 ◽  
Vol 125 (1) ◽  
pp. 33-39 ◽  
Author(s):  
T. Hadrys ◽  
T. Braun ◽  
S. Rinkwitz-Brandt ◽  
H.H. Arnold ◽  
E. Bober
Keyword(s):  
Homologous Recombination ◽  
Inner Ear ◽  
Homeobox Gene ◽  
Semicircular Canals ◽  
Otic Vesicle ◽  
Null Mutation ◽  
Complex Structures ◽  
Vestibular Organ ◽  
Inner Ear Development ◽  
Vestibular Organs

The inner ear develops from the otic vesicle, a one-cell-thick epithelium, which eventually transforms into highly complex structures including the sensory organs for balance (vestibulum) and hearing (cochlea). Several mouse inner ear mutations with hearing and balance defects have been described but for most the underlying genes have not been identified, for example, the genes controlling the development of the vestibular organs. Here, we report the inactivation of the homeobox gene, Nkx5-1, by homologous recombination in mice. This gene is expressed in vestibular structures throughout inner ear development. Mice carrying the Nkx5-1 null mutation exhibit behavioural abnormalities that resemble the typical hyperactivity and circling movements of the shaker/waltzer type mutants. The balance defect correlates with severe malformations of the vestibular organ in Nkx5-1(−/−) mutants, which fail to develop the semicircular canals. Nkx5-1 is the first ear-specific molecule identified to play a crucial role in the formation of the mammalian vestibular system.

Mutations affecting development of the zebrafish inner ear and lateral line

Development ◽  
1996 ◽  
Vol 123 (1) ◽  
pp. 241-254 ◽  
Author(s):  
T.T. Whitfield ◽  
M. Granato ◽  
F.J. van Eeden ◽  
U. Schach ◽  
M. Brand ◽  
...  
Keyword(s):  
Inner Ear ◽  
Lateral Line ◽  
Large Scale ◽  
Sensory System ◽  
Semicircular Canals ◽  
Abnormal Development ◽  
Pigment Cells ◽  
Otic Vesicle ◽  
In The Wild ◽  
Complementation Groups

Mutations giving rise to anatomical defects in the inner ear have been isolated in a large scale screen for mutations causing visible abnormalities in the zebrafish embryo (Haffter, P., Granato, M., Brand, M. et al. (1996) Development 123, 1–36). 58 mutants have been classified as having a primary ear phenotype; these fall into several phenotypic classes, affecting presence or size of the otoliths, size and shape of the otic vesicle and formation of the semicircular canals, and define at least 20 complementation groups. Mutations in seven genes cause loss of one or both otoliths, but do not appear to affect development of other structures within the ear. Mutations in seven genes affect morphology and patterning of the inner ear epithelium, including formation of the semicircular canals and, in some, development of sensory patches (maculae and cristae). Within this class, dog-eared mutants show abnormal development of semicircular canals and lack cristae within the ear, while in van gogh, semicircular canals fail to form altogether, resulting in a tiny otic vesicle containing a single sensory patch. Both these mutants show defects in the expression of homeobox genes within the otic vesicle. In a further class of mutants, ear size is affected while patterning appears to be relatively normal; mutations in three genes cause expansion of the otic vesicle, while in little ears and microtic, the ear is abnormally small, but still contains all five sensory patches, as in the wild type. Many of the ear and otolith mutants show an expected behavioural phenotype: embryos fail to balance correctly, and may swim on their sides, upside down, or in circles. Several mutants with similar balance defects have also been isolated that have no obvious structural ear defect, but that may include mutants with vestibular dysfunction of the inner ear (Granato, M., van Eeden, F. J. M., Schach, U. et al. (1996) Development, 123, 399–413,). Mutations in 19 genes causing primary defects in other structures also show an ear defect. In particular, ear phenotypes are often found in conjunction with defects of neural crest derivatives (pigment cells and/or cartilaginous elements of the jaw). At least one mutant, dog-eared, shows defects in both the ear and another placodally derived sensory system, the lateral line, while hypersensitive mutants have additional trunk lateral line organs.

scholarly journals Microfluidic communicating vessel chip for expedited and automated immunomagnetic assays

Lab on a Chip ◽  
2018 ◽  
Vol 18 (24) ◽  
pp. 3830-3839 ◽  
Author(s):  
Yang Yang ◽  
Yong Zeng
Keyword(s):  
Hydrostatic Pressure ◽  
Simple Device ◽  
Pressure Driven Flow ◽  
Pressure Driven

A simple device exploits hydrostatic pressure-driven flow to simplify and expedite the immunoassay workflow.

scholarly journals Spemann organizer gene Goosecoid promotes delamination of neuroblasts from the otic vesicle

2016 ◽  
Vol 113 (44) ◽  
pp. E6840-E6848 ◽  
Author(s):  
Husniye Kantarci ◽  
Andrea Gerberding ◽  
Bruce B. Riley
Keyword(s):  
Inner Ear ◽  
Epithelial To Mesenchymal Transition ◽  
Otic Vesicle ◽  
General Function ◽  
Cellular Dynamics ◽  
Mesenchymal Transition ◽  
Spemann Organizer ◽  
Developmental Role ◽  
Overlapping Domains ◽  
Low Incidence

Neurons of the Statoacoustic Ganglion (SAG), which innervate the inner ear, originate as neuroblasts in the floor of the otic vesicle and subsequently delaminate and migrate toward the hindbrain before completing differentiation. In all vertebrates, locally expressed Fgf initiates SAG development by inducing expression of Neurogenin1 (Ngn1) in the floor of the otic vesicle. However, not all Ngn1-positive cells undergo delamination, nor has the mechanism controlling SAG delamination been elucidated. Here we report that Goosecoid (Gsc), best known for regulating cellular dynamics in the Spemann organizer, regulates delamination of neuroblasts in the otic vesicle. In zebrafish, Fgf coregulates expression of Gsc and Ngn1 in partially overlapping domains, with delamination occurring primarily in the zone of overlap. Loss of Gsc severely inhibits delamination, whereas overexpression of Gsc greatly increases delamination. Comisexpression of Ngn1 and Gsc induces ectopic delamination of some cells from the medial wall of the otic vesicle but with a low incidence, suggesting the action of a local inhibitor. The medial marker Pax2a is required to restrict the domain of gsc expression, and misexpression of Pax2a is sufficient to block delamination and fully suppress the effects of Gsc. The opposing activities of Gsc and Pax2a correlate with repression or up-regulation, respectively, of E-cadherin (cdh1). These data resolve a genetic mechanism controlling delamination of otic neuroblasts. The data also elucidate a developmental role for Gsc consistent with a general function in promoting epithelial-to-mesenchymal transition (EMT).

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