In VivoElectroporation and Time‐Lapse Imaging of the Rostral Migratory Stream in Developing Rodent Brain

2019 ◽  
Vol 87 (1) ◽  
pp. e65
Author(s):  
Zhihui Huang ◽  
Ying Wang
eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Cedric Bressan ◽  
Alessandra Pecora ◽  
Dave Gagnon ◽  
Marina Snapyan ◽  
Simon Labrecque ◽  
...  

Cell migration is a dynamic process that entails extensive protein synthesis and recycling, structural remodeling, and considerable bioenergetic demand. Autophagy is one of the pathways that maintain cellular homeostasis. Time-lapse imaging of autophagosomes and ATP/ADP levels in migrating cells in the rostral migratory stream of mouse revealed that decreases in ATP levels force cells into the stationary phase and induce autophagy. Pharmacological or genetic impairments of autophagy in neuroblasts using either bafilomycin, inducible conditional mice, or CRISPR/Cas9 gene editing decreased cell migration due to the longer duration of the stationary phase. Autophagy is modulated in response to migration-promoting and inhibiting molecular cues and is required for the recycling of focal adhesions. Our results show that autophagy and energy consumption act in concert in migrating cells to dynamically regulate the pace and periodicity of the migratory and stationary phases to sustain neuronal migration.


Acta Naturae ◽  
2016 ◽  
Vol 8 (3) ◽  
pp. 88-96
Author(s):  
Yu. K. Doronin ◽  
I. V. Senechkin ◽  
L. V. Hilkevich ◽  
M. A. Kurcer

In order to estimate the diversity of embryo cleavage relatives to embryo progress (blastocyst formation), time-lapse imaging data of preimplantation human embryo development were used. This retrospective study is focused on the topographic features and time parameters of the cleavages, with particular emphasis on the lengths of cleavage cycles and the genealogy of blastomeres in 2- to 8-cell human embryos. We have found that all 4-cell human embryos have four developmental variants that are based on the sequence of appearance and orientation of cleavage planes during embryo cleavage from 2 to 4 blastomeres. Each variant of cleavage shows a strong correlation with further developmental dynamics of the embryos (different cleavage cycle characteristics as well as lengths of blastomere cycles). An analysis of the sequence of human blastomere divisions allowed us to postulate that the effects of zygotic determinants are eliminated as a result of cleavage, and that, thereafter, blastomeres acquire the ability of own syntheses, regulation, polarization, formation of functional contacts, and, finally, of specific differentiation. This data on the early development of human embryos obtained using noninvasive methods complements and extend our understanding of the embryogenesis of eutherian mammals and may be applied in the practice of reproductive technologies.


2019 ◽  
Vol 1 ◽  
pp. 204-210 ◽  
Author(s):  
Alyson Wilson ◽  
Stanley Serafin ◽  
Dilan Seckiner ◽  
Rachel Berry ◽  
Xanthé Mallett

2021 ◽  
Vol 109 ◽  
pp. 103363
Author(s):  
Ben Roche ◽  
Jonathan M. Bull ◽  
Hector Marin-Moreno ◽  
Timothy G. Leighton ◽  
Ismael H. Falcon-Suarez ◽  
...  

2016 ◽  
Vol 10 (1) ◽  
pp. 174-184 ◽  
Author(s):  
Sajith Kecheril Sadanandan ◽  
Ozden Baltekin ◽  
Klas E. G. Magnusson ◽  
Alexis Boucharin ◽  
Petter Ranefall ◽  
...  

2017 ◽  
Vol 36 (5) ◽  
pp. 519-528 ◽  
Author(s):  
Tomoyo Tanaka ◽  
Mitsuhiro Hoshijima ◽  
Junko Sunaga ◽  
Takashi Nishida ◽  
Mana Hashimoto ◽  
...  

2021 ◽  
Vol 7 (3) ◽  
pp. eabe3882
Author(s):  
Jenny F. Nathans ◽  
James A. Cornwell ◽  
Marwa M. Afifi ◽  
Debasish Paul ◽  
Steven D. Cappell

The G1-S checkpoint is thought to prevent cells with damaged DNA from entering S phase and replicating their DNA and efficiently arrests cells at the G1-S transition. Here, using time-lapse imaging and single-cell tracking, we instead find that DNA damage leads to highly variable and divergent fate outcomes. Contrary to the textbook model that cells arrest at the G1-S transition, cells triggering the DNA damage checkpoint in G1 phase route back to quiescence, and this cellular rerouting can be initiated at any point in G1 phase. Furthermore, we find that most of the cells receiving damage in G1 phase actually fail to arrest and proceed through the G1-S transition due to persistent cyclin-dependent kinase (CDK) activity in the interval between DNA damage and induction of the CDK inhibitor p21. These observations necessitate a revised model of DNA damage response in G1 phase and indicate that cells have a G1 checkpoint.


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