THE ROLE OF ENDO-1,4-BETA-GLUCANASE IN PLANT CELL ELONGATION. IN-VITRO STUDIES OF PEACH POLLEN

The otocyst is the epithelial anlage of the membranous labyrinth which interacts with surrounding cephalic mesenchyme to form an otic capsule. A series of in vitro studies was performed to gain a better understanding of the epithelial—mesenchymal interactions involved in this process. Parallel series of otocyst/mesenchyme (O/M) and isolated periotic mesenchyme (M) explants provided morphological and biochemical data to define the role of the otocyst in organizing and directing formation of its cartilaginous otic capsule. Explants were made from mouse embryos ranging in age from 10 to 14 days of gestation, and organ cultured under identical conditions until the chronological equivalent of 16 days of gestation. Expression of chrondrogenesis was determined by both histology and biochemistry. The in vitro behaviour of periotic mesenchyme explanted either with or without an otocyst supports several hypotheses that explain aspects of otic capsule development. The results indicate that (a) prior to embryonic day 12 the otocyst alone is not sufficient to stimulate chondrogenesis of the otic capsule within O/M explants; (b) the otocyst acts as an inductor of capsule chondrogenesis within O/M explants between embryonic days 12 to 13; (c) isolated mesenchyme within M explants taken from 13-day-old embryos are capable of initiating in vitro chondrogenesis, but without expressing capsule morphology in the absence of the otocyst; and (d) the isolated mesenchyme of M explants obtained from 14-day-old embryos expresses both chondrogenesis and otic capsule morphology in the absence of the otocyst. These findings suggest that the otocyst acts as an inductor of chondrogenesis of periotic mesenchyme tissue between embryonic days 11 to 13, and controls capsular morphogenesis between embryonic days 13 to 14 in the mouse embryo.

Download Full-text

A critical role of VLA-4 in erythropoiesis in vivo

Blood ◽

10.1182/blood.v87.6.2513.bloodjournal8762513 ◽

1996 ◽

Vol 87 (6) ◽

pp. 2513-2517 ◽

Cited By ~ 54

Author(s):

K Hamamura ◽

H Matsuda ◽

Y Takeuchi ◽

S Habu ◽

H Yagita ◽

...

Keyword(s):

Monoclonal Antibody ◽

Fetal Liver ◽

Critical Role ◽

In Utero ◽

In Vitro Studies ◽

Specific Interactions ◽

Erythroid Progenitors

Hematopoiesis requires specific interactions with the microenvironments, and VLA-4 has been implicated in these interactions based on in vitro studies. To study the role of VLA-4 in hematopoiesis in vivo, we performed in utero treatment of mice with an anti-VLA-4 monoclonal antibody. Although all hematopoietic cells in fetal liver expressed VLA-4, the treatment specifically induced anemia. It had no effect on the development of nonerythroid lineage cells, including lymphoids and myeloids. In the treated liver almost no erythroblast was detected, whereas the erythroid progenitors, which give rise to erythroid colonies in vitro, were present. These results indicate that VLA-4 plays a critical role in erythropoiesis, while it is not critical in lymphopoiesis in vivo.

Download Full-text

The role of BH3-only protein Bim extends beyond inhibiting Bcl-2–like prosurvival proteins

The Journal of Cell Biology ◽

10.1083/jcb.200905153 ◽

2009 ◽

Vol 186 (3) ◽

pp. 355-362 ◽

Cited By ~ 131

Author(s):

Delphine Mérino ◽

Maybelline Giam ◽

Peter D. Hughes ◽

Owen M. Siggs ◽

Klaus Heger ◽

...

Keyword(s):

Family Members ◽

Binding Specificity ◽

In Vitro Studies ◽

Genetic Approach ◽

Activation Model ◽

Bh3 Domain ◽

Indirect Activation

Proteins of the Bcl-2 family are critical regulators of apoptosis, but how its BH3-only members activate the essential effectors Bax and Bak remains controversial. The indirect activation model suggests that they simply must neutralize all of the prosurvival Bcl-2 family members, whereas the direct activation model proposes that Bim and Bid must activate Bax and Bak directly. As numerous in vitro studies have not resolved this issue, we have investigated Bim's activity in vivo by a genetic approach. Because the BH3 domain determines binding specificity for Bcl-2 relatives, we generated mice having the Bim BH3 domain replaced by that of Bad, Noxa, or Puma. The mutants bound the expected subsets of prosurvival relatives but lost interaction with Bax. Analysis of the mice showed that Bim's proapoptotic activity is not solely caused by its ability to engage its prosurvival relatives or solely to its binding to Bax. Thus, initiation of apoptosis in vivo appears to require features of both models.

Download Full-text