scholarly journals Why do curly tail lizards (genusLeiocephalus) curl their tails? An assessment of displays toward conspecifics and predators

Ethology ◽  
2017 ◽  
Vol 123 (5) ◽  
pp. 342-347 ◽  
Author(s):  
Bonnie K. Kircher ◽  
Michele A. Johnson
Keyword(s):  
Curly Tail

Genesis and prevention of spinal neural tube defects in the curly tail mutant mouse: involvement of retinoic acid and its nuclear receptors RAR-beta and RAR-gamma

Development ◽  
1995 ◽  
Vol 121 (3) ◽  
pp. 681-691
Author(s):  
W.H. Chen ◽  
G.M. Morriss-Kay ◽  
A.J. Copp
Keyword(s):  
Retinoic Acid ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
In Situ Hybridisation ◽  
Tail Bud ◽  
Retinoic Acid Signalling ◽  
All Trans Retinoic Acid ◽  
Posterior Neuropore ◽  
Computerised Image Analysis ◽  
Curly Tail

A role for all-trans-retinoic acid in spinal neurulation is suggested by: (1) the reciprocal domains of expression of the retinoic acid receptors RAR-beta and RAR-gamma in the region of the closed neural tube and open posterior neuropore, respectively, and (2) the preventive effect of maternally administered retinoic acid (5 mg/kg) on spinal neural tube defects in curly tail (ct/ct) mice. Using in situ hybridisation and computerised image analysis we show here that in ct/ct embryos, RAR-beta transcripts are deficient in the hindgut endoderm, a tissue whose proliferation rate is abnormal in the ct mutant, and RAR-gamma transcripts are deficient in the tail bud and posterior neuropore region. The degree of deficiency of RAR-gamma transcripts is correlated with the severity of delay of posterior neuropore closure. As early as 2 hours following RA treatment at 10 days 8 hours post coitum, i.e. well before any morphogenetic effects are detectable, RAR-beta expression is specifically upregulated in the hindgut endoderm, and the abnormal expression pattern of RAR-gamma is also altered. These results suggest that the spinal neural tube defects which characterise the curly tail phenotype may be due to interaction between the ct gene product and one or more aspects of the retinoic acid signalling pathway.

Neural tube development in mutant (curly tail) and normal mouse embryos: the timing of posterior neuropore closure in vivo and in vitro

Development ◽  
1982 ◽  
Vol 69 (1) ◽  
pp. 151-167
Author(s):  
A. J. Copp ◽  
M. J. Seller ◽  
P. E. Polani
Keyword(s):  
Neural Tube ◽  
Neural Tube Defects ◽  
Mouse Embryos ◽  
Injection Technique ◽  
Posterior Neuropore ◽  
Curly Tail ◽  
Mechanisms Of Development ◽  
Delayed Closure

A dye-injection technique has been used to determine the developmental stage at which posterior neuropore (PNP) closure occurs in normal and mutant curly tail mouse embryos. In vivo, the majority of non-mutant embryos undergo PNP closure between 30 and 34 somites whereas approximately 50% of all mutant embryos show delayed closure, and around 20% maintain an open PNP even at advanced stages of development. A similar result has been found for embryos developing in vitro from the headfold stage. Later in development, 50–60% of mutant embryos in vivo develop tail flexion defects, and 15–20% lumbosacral myeloschisis. This supports the view that delayed PNP closure is the main developmental lesion leading to the appearance of caudal neural tube defects in curly tail mice. The neural tube is closed in the region of tail flexion defects, but it is locally overexpanded and abnormal in position. The significance of these observations is discussed in relation to possible mechanisms of development of lumbosacral and caudal neural tube defects. This paper constitutes the first demonstration of the development of a genetically induced malformation in vitro.

scholarly journals Reduced Glucose Consumption in the Curly Tail Mouse Does Not Initiate the Pathogenesis Leading to Spinal Neural Tube Defects

1998 ◽  
Vol 128 (10) ◽  
pp. 1819-1828 ◽  
Author(s):  
Marian C. E. Peeters ◽  
Jan L.M.C. Geelen ◽  
Johan W. M. Hekking ◽  
Niels Chavannes ◽  
Joep P. M. Geraedts ◽  
...  
Keyword(s):  
Neural Tube ◽  
Neural Tube Defects ◽  
Glucose Consumption ◽  
Curly Tail

A Curly-Tail Modifier Locus,mct1,on Mouse Chromosome 17

Genomics ◽  
1995 ◽  
Vol 29 (3) ◽  
pp. 719-724 ◽  
Author(s):  
VERITY A. LETTS ◽  
NICHOLAS J. SCHORK ◽  
ANDREW J. COPP ◽  
MERTON BERNFIELD ◽  
WAYNE N. FRANKEL
Keyword(s):  
Mouse Chromosome ◽  
Chromosome 17 ◽  
Modifier Locus ◽  
Curly Tail

scholarly journals Arl13b and the exocyst interact synergistically in ciliogenesis

2016 ◽  
Vol 27 (2) ◽  
pp. 308-320 ◽  
Author(s):  
Cecília Seixas ◽  
Soo Young Choi ◽  
Noemi Polgar ◽  
Nicole L. Umberger ◽  
Michael P. East ◽  
...  
Keyword(s):  
Kidney Development ◽  
Genetic Interaction ◽  
Joubert Syndrome ◽  
Conditional Knockout ◽  
Multiple Organs ◽  
Conditional Deletion ◽  
Curly Tail ◽  
Adp Ribosylation Factor ◽  
Precise Role

Arl13b belongs to the ADP-ribosylation factor family within the Ras superfamily of regulatory GTPases. Mutations in Arl13b cause Joubert syndrome, which is characterized by congenital cerebellar ataxia, hypotonia, oculomotor apraxia, and mental retardation. Arl13b is highly enriched in cilia and is required for ciliogenesis in multiple organs. Nevertheless, the precise role of Arl13b remains elusive. Here we report that the exocyst subunits Sec8, Exo70, and Sec5 bind preferentially to the GTP-bound form of Arl13b, consistent with the exocyst being an effector of Arl13b. Moreover, we show that Arl13b binds directly to Sec8 and Sec5. In zebrafish, depletion of arl13b or the exocyst subunit sec10 causes phenotypes characteristic of defective cilia, such as curly tail up, edema, and abnormal pronephric kidney development. We explored this further and found a synergistic genetic interaction between arl13b and sec10 morphants in cilia-dependent phenotypes. Through conditional deletion of Arl13b or Sec10 in mice, we found kidney cysts and decreased ciliogenesis in cells surrounding the cysts. Moreover, we observed a decrease in Arl13b expression in the kidneys from Sec10 conditional knockout mice. Taken together, our results indicate that Arl13b and the exocyst function together in the same pathway leading to functional cilia.

scholarly journals Curly tail: a 50-year history of the mouse spina bifida model

2001 ◽  
Vol 203 (4) ◽  
pp. 225-238 ◽  
Author(s):  
H. W. M. van Straaten ◽  
Andrew J. Copp
Keyword(s):  
Spina Bifida ◽  
Curly Tail ◽  
History Of

Quantification of the closure delay of the neural tube in the curly tail mouse embryo

1989 ◽  
Vol 27 ◽  
pp. 201
Author(s):  
H.W.M. van Straaten ◽  
A. Copp ◽  
M.R. Bernfield
Keyword(s):  
Neural Tube ◽  
Mouse Embryo ◽  
Curly Tail

An ablative postposition in the Xining dialect

1999 ◽  
Vol 11 (1) ◽  
pp. 1-17 ◽  
Author(s):  
Keith Dede
Keyword(s):  
Language Contact ◽  
Demographic Changes ◽  
Linguistic Change ◽  
Curly Tail ◽  
Chinese Dialects ◽  
Neutral Tone ◽  
Morphosyntactic Feature

This article describes a morphosyntactic feature of the Xining dialect that is unique among all Chinese dialects: that is, the use of a postposition to express ablative nominal relationships. The postposition [t[curly-tail lowercase c]ia] is invariably pronounced in the neutral tone and has no cognates in either earlier varieties of Chinese or among present Chinese dialects. The morpheme's origin is shown to have come from a neighboring non-Sinitic language. Moreover, the variations within the syntactic expression of the ablative are correlated with various sociolinguistic groups. These correlations suggest an ongoing change in the dialect's morphosyntactic system of a kind rarely observed among Chinese dialects. Finally, the process of linguistic change is correlated with demographic changes within the Xining region that show Xining is a place where language contact and rapid linguistic change are likely to be found.

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