scholarly journals In vivo time-lapse analysis of cell divisions during neural tube closure

2006 ◽  
Vol 295 (1) ◽  
pp. 444
Author(s):  
Esther K. Kieserman ◽  
Julian M. Tyszka ◽  
John B. Wallingford
Keyword(s):  
Neural Tube ◽  
Time Lapse ◽  
Neural Tube Closure ◽  
Cell Divisions ◽  
Tube Closure

scholarly journals Live imaging of apoptosis in a novel transgenic mouse highlights its role in neural tube closure

2011 ◽  
Vol 195 (6) ◽  
pp. 1047-1060 ◽  
Author(s):  
Yoshifumi Yamaguchi ◽  
Naomi Shinotsuka ◽  
Keiko Nonomura ◽  
Kiwamu Takemoto ◽  
Keisuke Kuida ◽  
...  
Keyword(s):  
Transgenic Mouse ◽  
Neural Tube ◽  
Resonance Energy Transfer ◽  
Resonance Energy ◽  
Time Lapse ◽  
Neural Tube Closure ◽  
Caspase Activation ◽  
Fluorescent Reporter ◽  
Time Lapse Imaging ◽  
Tube Closure

Many cells die during development, tissue homeostasis, and disease. Dysregulation of apoptosis leads to cranial neural tube closure (NTC) defects like exencephaly, although the mechanism is unclear. Observing cells undergoing apoptosis in a living context could help elucidate their origin, behavior, and influence on surrounding tissues, but few tools are available for this purpose, especially in mammals. In this paper, we used insulator sequences to generate a transgenic mouse that stably expressed a genetically encoded fluorescence resonance energy transfer (FRET)–based fluorescent reporter for caspase activation and performed simultaneous time-lapse imaging of apoptosis and morphogenesis in living embryos. Live FRET imaging with a fast-scanning confocal microscope revealed that cells containing activated caspases showed typical and nontypical apoptotic behavior in a region-specific manner during NTC. Inhibiting caspase activation perturbed and delayed the smooth progression of cranial NTC, which might increase the risk of exencephaly. Our results suggest that caspase-mediated cell removal facilitates NTC completion within a limited developmental window.

Curvature of the caudal region is responsible for failure of neural tube closure in the curly tail (ct) mouse embryo

Development ◽  
1991 ◽  
Vol 113 (2) ◽  
pp. 671-678 ◽  
Author(s):  
F.A. Brook ◽  
A.S. Shum ◽  
H.W. Van Straaten ◽  
A.J. Copp
Keyword(s):  
Neural Tube ◽  
Mouse Embryo ◽  
Mouse Embryos ◽  
The Body ◽  
Neural Tube Closure ◽  
Posterior Neuropore ◽  
Curly Tail ◽  
Delayed Closure ◽  
Tube Closure

Delayed closure of the posterior neuropore (PNP) occurs to a variable extent in homozygous mutant curly tail (ct) mouse embryos, and results in the development of spinal neural tube defects (NTD) in 60% of embryos. Previous studies have suggested that curvature of the body axis may delay neural tube closure in the cranial region of the mouse embryo. In order to investigate the relationship between curvature and delayed PNP closure, we measured the extent of ventral curvature of the neuropore region in ct/ct embryos with normal or delayed PNP closure. The results show significantly greater curvature in ct/ct embryos with delayed PNP closure in vivo than in their normal littermates. Reopening of the posterior neuropore in non-mutant mouse embryos, to delay neuropore closure experimentally, did not increase ventral curvature, suggesting that increased curvature in ct/ct embryos is not likely to be a secondary effect of delayed PNP closure. Experimental prevention of ventral curvature in ct/ct embryos, brought about by implantation of an eyelash tip longitudinally into the hindgut lumen, ameliorated the delay in PNP closure. We propose, therefore, that increased ventral curvature of the neuropore region of ct/ct embryos imposes a mechanical stress, which opposes neurulation and thus delays closure of the PNP. Increased ventral curvature may arise as a result of a cell proliferation imbalance, which we demonstrated previously in affected ct/ct embryos.

scholarly journals Global analysis of cell behavior and protein localization dynamics reveals region-specific functions for Shroom3 and N-cadherin during neural tube closure

2021 ◽  
Author(s):  
Austin T. Baldwin ◽  
Juliana Kim ◽  
John B. Wallingford
Keyword(s):  
Neural Tube ◽  
Cell Biology ◽  
Protein Localization ◽  
Global Analysis ◽  
Time Lapse ◽  
Tissue Level ◽  
Neural Tube Closure ◽  
Cell Behaviors ◽  
Regional Specificity ◽  
Tube Closure

AbstractFailures of neural tube closure are common and serious birth defects, yet we have a poor understanding of the interaction of genetics and cell biology during neural tube closure. Additionally, mutations that cause neural tube defects (NTDs) tend to affect anterior or posterior regions of the neural tube but rarely both, indicating a regional specificity to NTD genetics. To better understand the regional specificity of cell behaviors during neural tube closure, we analyzed the dynamic localization of actin and N-cadherin via high-resolution tissue-level time-lapse microscopy during Xenopus neural tube closure. To investigate the regionality of gene function, we generated mosaic mutations in shroom3, a key regulator or neural tube closure This approach elucidates new differences between cell behaviors during cranial/anterior and spinal/posterior neural tube closure, provides mechanistic insight into the function of shroom3 and demonstrates the ability of tissue-level imaging and analysis to generate cell-biological mechanistic insights into neural tube closure.

scholarly journals Defective Neural Tube Closure and Anteroposterior Patterning in Mice Lacking the LIM Protein LMO4 or Its Interacting Partner Deaf-1

2004 ◽  
Vol 24 (5) ◽  
pp. 2074-2082 ◽  
Author(s):  
Kyungmin Hahm ◽  
Eleanor Y. M. Sum ◽  
Yuko Fujiwara ◽  
Geoffrey J. Lindeman ◽  
Jane E. Visvader ◽  
...  
Keyword(s):  
Neural Tube ◽  
Cranial Nerves ◽  
Transcriptional Regulators ◽  
Neural Tube Closure ◽  
Incomplete Penetrance ◽  
Anteroposterior Patterning ◽  
Rib Cage ◽  
Skeletal Defects ◽  
Tube Closure

ABSTRACT LMO4 belongs to a family of transcriptional regulators that comprises two zinc-binding LIM domains. LIM-only (LMO) proteins appear to function as docking sites for other factors, leading to the assembly of multiprotein complexes. The transcription factor Deaf-1/NUDR has been identified as one partner protein of LMO4. We have disrupted the Lmo4 and Deaf-1 genes in mice to define their biological function in vivo. All Lmo4 mutants died shortly after birth and showed defects within the presphenoid bone, with 50% of mice also exhibiting exencephaly. Homeotic transformations were observed in Lmo4-null embryos and newborn mice, but with incomplete penetrance. These included skeletal defects in cervical vertebrae and the rib cage. Furthermore, fusions of cranial nerves IX and X and defects in cranial nerve V were apparent in some Lmo4−/− and Lmo4+/− mice. Remarkably, Deaf-1 mutants displayed phenotypic abnormalities similar to those observed in Lmo4 mutants. These included exencephaly, transformation of cervical segments, and rib cage abnormalities. In contrast to Lmo4 nullizygous mice, nonexencephalic Deaf-1 mutants remained healthy. No defects in the sphenoid bone or cranial nerves were apparent. Thus, Lmo4 and Deaf-1 mutant mice exhibit overlapping as well as distinct phenotypes. Our data indicate an important role for these two transcriptional regulators in pathways affecting neural tube closure and skeletal patterning, most likely reflecting their presence in a functional complex in vivo.

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