scholarly journals Controlled Neighbor Exchanges Drive Glassy Behavior, Intermittency, and Cell Streaming in Epithelial Tissues

2021 ◽  
Vol 11 (4) ◽  
Author(s):  
Amit Das ◽  
Srikanth Sastry ◽  
Dapeng Bi
Genetics ◽  
1997 ◽  
Vol 147 (1) ◽  
pp. 243-253 ◽  
Author(s):  
Joseph Jack ◽  
Guy Myette

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.


2015 ◽  
Vol 92 (18) ◽  
Author(s):  
Adam Berlie ◽  
Ian Terry ◽  
Marek Szablewski ◽  
Sean R. Giblin

2016 ◽  
Vol 85 (9) ◽  
pp. 094712
Author(s):  
Junjie Yang ◽  
Anjana M. Samarakoon ◽  
Kyun Woo Hong ◽  
John R. D. Copley ◽  
Qingzhen Huang ◽  
...  

2007 ◽  
Vol 92 (10) ◽  
pp. 3941-3948
Author(s):  
Stephanie C. Hsu ◽  
Joshua D. Groman ◽  
Christian A. Merlo ◽  
Kathleen Naughton ◽  
Pamela L. Zeitlin ◽  
...  

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.


1988 ◽  
Vol 27 (Part 2, No. 2) ◽  
pp. L132-L133 ◽  
Author(s):  
Shinji Matsuo ◽  
Hiroyuki Nasu ◽  
Chikashi Akamatsu ◽  
Ryo Hayashi ◽  
Takeshi Imura ◽  
...  
Keyword(s):  

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

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

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