vascular formation
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Author(s):  
Ken-ichi Kurotani ◽  
Michitaka Notaguchi

Abstract Grafting is a means to connect tissues from two individual plants and grow a single chimeric plant through establishment of both apoplasmic and symplasmic connections. Recent molecular studies using RNA-sequencing data have provided genetic information on the processes involved in tissue reunion, including wound response, cell division, cell-cell adhesion, cell differentiation, and vascular formation. Thus, studies on grafting increase our understanding of various aspects of plant biology. Grafting has also been used to study systemic signaling and transport of micro- and macromolecules in the plant body. Given that graft viability and molecular transport across graft junctions largely depend on vascular formation, a major focus in grafting biology has been the mechanism of vascular development. In addition, it has been thought that symplasmic connections via plasmodesmata are fundamentally important to share cellular information among newly proliferated cells at the graft interface and to accomplish tissue differentiation correctly. Therefore, this review focuses on plasmodesmata formation during grafting. We take advantage of interfamily grafts for unambiguous identification of the graft interface and summarize morphological aspects of de novo formation of plasmodesmata. Important molecular events are addressed by re-examining the time-course transcriptome of interfamily grafts, from which we recently identified the cell-cell adhesion mechanism. Plasmodesmata-associated genes upregulated during graft healing that may provide a link to symplasm establishment are described. We also discuss future research directions.


2021 ◽  
Author(s):  
Shinji Itoh ◽  
Tomoharu Yoshizumi ◽  
Yoshiyuki Kitamura ◽  
Kyohei Yugawa ◽  
Norifumi Iseda ◽  
...  

genesis ◽  
2021 ◽  
Author(s):  
Yumi Kinugasa‐Katayama ◽  
Yusuke Watanabe ◽  
Takashi Hisamitsu ◽  
Yuichiro Arima ◽  
Norika M. Liu ◽  
...  

2020 ◽  
Vol 23 (4) ◽  
pp. 202-207
Author(s):  
Azizzhon D. Zikiryachodzhaev ◽  
E. K. Saribekyan ◽  
E. Yu. Vertieva ◽  
I. S. Pestin

INTRODUCTION:Nodular melanoma is a rapidly progressive skin tumour with a high risk of methastasis even on early stages. This fact leads to necessity of non-invasive procedures, which can verify this diagnosis before surgery. Nodular forms of amelanotic melanoma can be hardly diagnosed because of their unusual diagnostic and dermatoscopic features. CASE REPORT:Pyogenic granuloma is the most difficult disease for differential diagnosis. It is a benign vascular formation, which mimics nodular amelanotic melanoma.


2020 ◽  
Author(s):  
Tomomi Matsukura ◽  
Chisato Kataoka ◽  
Yohei Kawana ◽  
Misato Fujita ◽  
Shosaku Kashiwada

Hepatology ◽  
2020 ◽  
Vol 72 (6) ◽  
pp. 1987-1999 ◽  
Author(s):  
Shinji Itoh ◽  
Tomoharu Yoshizumi ◽  
Kyohei Yugawa ◽  
Daisuke Imai ◽  
Shohei Yoshiya ◽  
...  

2020 ◽  
Vol 295 (51) ◽  
pp. 17632-17645
Author(s):  
Yusuke Watanabe ◽  
Daiki Seya ◽  
Dai Ihara ◽  
Shuhei Ishii ◽  
Taiki Uemoto ◽  
...  

Thoracic great vessels such as the aorta and subclavian arteries are formed through dynamic remodeling of embryonic pharyngeal arch arteries (PAAs). Previous work has shown that loss of a basic helix-loop-helix transcription factor Hey1 in mice causes abnormal fourth PAA development and lethal great vessel anomalies resembling congenital malformations in humans. However, how Hey1 mediates vascular formation remains unclear. In this study, we revealed that Hey1 in vascular endothelial cells, but not in smooth muscle cells, played essential roles for PAA development and great vessel morphogenesis in mouse embryos. Tek-Cre–mediated Hey1 deletion in endothelial cells affected endothelial tube formation and smooth muscle differentiation in embryonic fourth PAAs and resulted in interruption of the aortic arch and other great vessel malformations. Cell specificity and signal responsiveness of Hey1 expression were controlled through multiple cis-regulatory regions. We found two distal genomic regions that had enhancer activity in endothelial cells and in the pharyngeal epithelium and somites, respectively. The novel endothelial enhancer was conserved across species and was specific to large-caliber arteries. Its transcriptional activity was regulated by Notch signaling in vitro and in vivo, but not by ALK1 signaling and other transcription factors implicated in endothelial cell specificity. The distal endothelial enhancer was not essential for basal Hey1 expression in mouse embryos but may likely serve for Notch-dependent transcriptional control in endothelial cells together with the proximal regulatory region. These findings help in understanding the significance and regulation of endothelial Hey1 as a mediator of multiple signaling pathways in embryonic vascular formation.


2020 ◽  
Vol 12 (2-4) ◽  
pp. 207
Author(s):  
M. Valente ◽  
S. Turoczi ◽  
P. Kantane ◽  
G. Marazzi ◽  
J.S. Hulot ◽  
...  
Keyword(s):  

Author(s):  
Xi Chen ◽  
Ryan Imperio ◽  
Kai R. Seely ◽  
Christian Viehland ◽  
Joseph A. Izatt ◽  
...  

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