Epithelial Tissues as Active Solids: From Nonlinear Contraction Pulses to Rupture Resistance

2020 ◽  
Author(s):  
Mariana De Niz
Keyword(s):  
Epithelial Tissues ◽  
Nonlinear Contraction

scholarly journals The Genes raw and ribbon Are Required for Proper Shape of Tubular Epithelial Tissues in Drosophila

Genetics ◽  
1997 ◽  
Vol 147 (1) ◽  
pp. 243-253 ◽  
Author(s):  
Joseph Jack ◽  
Guy Myette
Keyword(s):  
Embryonic Development ◽  
Salivary Glands ◽  
Cell Shape ◽  
Malpighian Tubules ◽  
Dorsal Closure ◽  
Epithelial Tissues ◽  
Cell Rearrangement

Abstract The products of two genes, raw and ribbon (rib), are required for the proper morphogenesis of a variety of tissues. Malpighian tubules mutant for raw or rib are wider and shorter than normal tubules, which are only two cells in circumference when they are fully formed. The mutations alter the shape of the tubules beginning early in their formation and block cell rearrangement late in development, which normally lengthens and narrows the tubes. Mutations of both genes affect a number of other tissues as well. Both genes are required for dorsal closure and retraction of the CNS during embryonic development. In addition, rib mutations block head involution, and broaden and shorten other tubular epithelia (salivary glands, tracheae, and hindgut) in much same manner as they alter the shape of the Malpighian tubules. In tissues in which the shape of cells can be observed readily, rib mutations alter cell shape, which probably causes the change in shape of the organs that are affected. In double mutants raw enhances the phenotypes of all the tissues that are affected by rib but unaffected by raw alone, indicating that raw is also active in these tissues.

scholarly journals Patients with Mutations in Gsα Have Reduced Activation of a Downstream Target in Epithelial Tissues due to Haploinsufficiency

2007 ◽  
Vol 92 (10) ◽  
pp. 3941-3948
Author(s):  
Stephanie C. Hsu ◽  
Joshua D. Groman ◽  
Christian A. Merlo ◽  
Kathleen Naughton ◽  
Pamela L. Zeitlin ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cells ◽  
G Protein ◽  
G Protein Signaling ◽  
Protein Signaling ◽  
Downstream Target ◽  
Epithelial Tissues ◽  
Stimulatory G Protein ◽  
Normal Controls

Abstract Context: Patients with Albright hereditary osteodystrophy (AHO) have defects in stimulatory G protein signaling due to loss of function mutations in GNAS. The mechanism by which these mutations lead to the AHO phenotype has been difficult to establish due to the inaccessibility of the affected tissues. Objective: The objective of the study was to gain insight into the downstream consequences of abnormal stimulatory G protein signaling in human epithelial tissues. Patients and Design: We assessed transcription of GNAS and Gsα-stimulated activation of the cystic fibrosis transmembrane conductance regulator (CFTR) in AHO patients, compared with normal controls and patients with cystic fibrosis. Main Outcome Measures: Relative expression of Gsα transcripts from each parental GNAS allele and cAMP measurements from nasal epithelial cells were compared among normal controls and AHO patients. In vivo measurements of CFTR function, pulmonary function, and pancreatic function were assessed in AHO patients. Results: GNAS was expressed equally from each allele in normals and two of five AHO patients. cAMP generation was significantly reduced in nasal respiratory epithelial cells from AHO patients, compared with normal controls (0.4 vs. 0.6, P = 0.0008). Activation of CFTR in vivo in nasal (P = 0.0065) and sweat gland epithelia (P = 0.01) of AHO patients was significantly reduced from normal. In three patients, the reduction in activity was comparable with patients with cystic fibrosis due to mutations in CFTR. Yet no AHO patients had pulmonary or pancreatic disease consistent with cystic fibrosis. Conclusions: In humans, haploinsufficiency of GNAS causes a significant reduction in the activation of the downstream target, CFTR, in vivo.

Conductance of epithelial tissues with particular reference to the frog's cornea and gastric mucosa

1973 ◽  
Vol 15 (5) ◽  
pp. 533-552 ◽  
Author(s):  
W.S. Rehm ◽  
R.L. Shoemaker ◽  
S.S. Sanders ◽  
J.T. Tarvin ◽  
J.A. Wright ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Epithelial Tissues

Relatively high rates of G:C → A:T transitions at CpG sites were observed in certain epithelial tissues including pancreas and submaxillary gland of adult big blue® mice

2013 ◽  
Vol 55 (1) ◽  
pp. 51-63 ◽  
Author(s):  
Anita Prtenjaca ◽  
Heather E. Tarnowski ◽  
Alison M. Marr ◽  
Melanie A. Heney ◽  
Laura Creamer ◽  
...  
Keyword(s):  
Submaxillary Gland ◽  
Cpg Sites ◽  
Epithelial Tissues

scholarly journals YAP Regulates the Expression ofHoxa1andHoxc13in Mouse and Human Oral and Skin Epithelial Tissues

2015 ◽  
Vol 35 (8) ◽  
pp. 1449-1461 ◽  
Author(s):  
Ming Liu ◽  
Shuangyun Zhao ◽  
Qingjie Lin ◽  
Xiu-Ping Wang
Keyword(s):  
Cell Proliferation ◽  
Expression Profiles ◽  
Tumor Development ◽  
Gene Expression Profiles ◽  
Tooth Germ ◽  
Conditional Knockout ◽  
Hippo Signaling ◽  
Embryonic Mouse ◽  
Downstream Targets ◽  
Epithelial Tissues

Yes-associated protein (YAP) is a Hippo signaling transcriptional coactivator that plays pivotal roles in stem cell proliferation, organ size control, and tumor development. The downstream targets of YAP have been shown to be highly context dependent. In this study, we used the embryonic mouse tooth germ as a tool to search for the downstream targets of YAP in ectoderm-derived tissues.Yapdeficiency in the dental epithelium resulted in a small tooth germ with reduced epithelial cell proliferation. We compared the gene expression profiles of embryonic day 14.5 (E14.5)Yapconditional knockout andYAPtransgenic mouse tooth germs using transcriptome sequencing (RNA-Seq) and further confirmed the differentially expressed genes using real-time PCR andin situhybridization. We found that YAP regulates the expression ofHoxa1andHoxc13in oral and dental epithelial tissues as well as in the epidermis of skin during embryonic and adult stages. Sphere formation assay suggested thatHoxa1andHoxc13are functionally involved in YAP-regulated epithelial progenitor cell proliferation, and chromatin immunoprecipitation (ChIP) assay implies that YAP may regulateHoxa1andHoxc13expression through TEAD transcription factors. These results provide mechanistic insights into abnormal YAP activities in mice and humans.

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