scholarly journals Thyroid hormone receptors in chick retinal development: differential expression of mRNAs for alpha and N-terminal variant beta receptors

Development ◽  
1992 ◽  
Vol 114 (1) ◽  
pp. 39-47 ◽  
Author(s):  
M. Sjoberg ◽  
B. Vennstrom ◽  
D. Forrest
Keyword(s):  
Thyroid Hormone ◽  
Hormone Receptors ◽  
Retinal Development ◽  
Outer Nuclear Layer ◽  
In Situ Hybridisation ◽  
Thyroid Hormone Receptors ◽  
Rat Pituitary ◽  
Beta 2 ◽  
Low Levels

Thyroid-hormone-dependent development of the neuroretina has principally been described in amphibia. Here, we show by in situ hybridisation that mRNAs coding for three distinct thyroid hormone receptors (TRs), TR alpha and two TR beta variants, are differentially expressed during chick retinal development. We isolated a cDNA for a novel N-terminal variant of chick TR beta (cTR beta 2) that is predominantly expressed in retinal development. Interestingly, in its N-terminal A/B domain cTR beta 2 is 70% homologous to the rat pituitary-specific TR beta 2. Expression of cTR beta 2 mRNA was high at embryonic day 6 (E6) in the retinal outer nuclear layer (ONL) and decreased to low levels at hatching. mRNA for the previously described chick beta receptor, cTR beta 0, was expressed at low levels in both the ONL and the inner nuclear layer (INL) after E10. In contrast, cTR alpha expression occurred in the ONL, INL and ganglion cell layer at intermediate and later stages. Finally, cTR beta 2 confers a stronger trans-activation of reporter gene transcription than cTR beta 0. The distinctive kinetics and localisation of TR alpha and beta gene expression suggest cell- and stage-specific functions for TRs, both individually and in combinations, in chick neuroretinal development.

scholarly journals Thyroid Hormone Receptors Control Developmental Maturation of the Middle Ear and the Size of the Ossicular Bones

Endocrinology ◽  
2012 ◽  
Vol 153 (3) ◽  
pp. 1548-1560 ◽  
Author(s):  
Emily A. Cordas ◽  
Lily Ng ◽  
Arturo Hernandez ◽  
Masahiro Kaneshige ◽  
Sheue-Yann Cheng ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Inner Ear ◽  
Middle Ear ◽  
Hormone Receptors ◽  
Dominant Negative ◽  
Thyroid Hormone Receptors ◽  
Auditory Thresholds ◽  
Auditory Development ◽  
Genes Encoding

Thyroid hormone is critical for auditory development and has well-known actions in the inner ear. However, less is known of thyroid hormone functions in the middle ear, which contains the ossicles (malleus, incus, stapes) that relay mechanical sound vibrations from the outer ear to the inner ear. During the later stages of middle ear development, prior to the onset of hearing, middle ear cavitation occurs, involving clearance of mesenchyme from the middle ear cavity while the immature cartilaginous ossicles attain appropriate size and ossify. Using in situ hybridization, we detected expression of Thra and Thrb genes encoding thyroid hormone receptors α1 and β (TRα1 and TRβ, respectively) in the immature ossicles, surrounding mesenchyme and tympanic membrane in the mouse. Thra+/PV mice that express a dominant-negative TRα1 protein exhibited deafness with elevated auditory thresholds and a range of middle ear abnormalities including chronic persistence of mesenchyme in the middle ear into adulthood, markedly enlarged ossicles, and delayed ossification of the ossicles. Congenitally hypothyroid Tshr−/− mice and TR-deficient Thra1−/−;Thrb−/− mice displayed similar abnormalities. These findings demonstrate that middle ear maturation is TR dependent and suggest that the middle ear is a sensitive target for thyroid hormone in development.

RNA and protein localisations of TGF beta 2 in the early mouse embryo suggest an involvement in cardiac development

Development ◽  
1993 ◽  
Vol 117 (2) ◽  
pp. 625-639 ◽  
Author(s):  
M.C. Dickson ◽  
H.G. Slager ◽  
E. Duffie ◽  
C.L. Mummery ◽  
R.J. Akhurst
Keyword(s):  
Cardiac Development ◽  
In Situ Hybridisation ◽  
Outflow Tract ◽  
Tgf Beta ◽  
Atrioventricular Canal ◽  
Whole Mount ◽  
Beta 2 ◽  
Low Levels ◽  
Early Mouse

We have performed a detailed analysis of the localisations of RNAs for TGF beta 2 and beta 3, and of TGF beta 2 protein in mouse embryos from 6.5 to 9.5 days post coitum, using in situ hybridisation and immunohistochemistry on serial sections, and whole-mount in situ hybridisation to complete embryos. TGF beta 3 RNA was not seen in any of the tissue sections, but very low levels of the RNA were seen by whole-mount in situ hybridisation around the outflow tract of the heart at 8.5 days post coitum. TGF beta 2 RNA is expressed at high levels in all cells with the potential to differentiate into cardiomyocytes. Additionally, the foregut endoderm, juxtaposed to the heart, and the neuroepithelium at the rostral extremity of the foregut, express very high levels of TGF beta 2 RNA, between 8.5 and 9.5 days post coitum. As cardiomyogenesis proceeds, TGF beta 2 RNA levels diminishes within the myocytes, with a concomitant increase in staining for TGF beta 2 protein. TGF beta 2 protein staining of cardiomyocytes persists throughout development and in the adult, in the absence of detectable levels of the corresponding RNA. Superimposed upon this myocardial pattern of expression, there is an upregulation of TGF beta 2 RNA in the myocardium of the outflow tract and atrioventricular canal between 8.5 and 9.5 days post coitum, which returns to low levels by 11.5 days post coitum. The results are discussed in terms of a potential role of TGF beta 2 in controlling cardiomyogenesis and in inductive interactions leading to cardiac cushion tissue formation.

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