L1-Type Cell Adhesion Molecules: Distinct Roles in Synaptic Targeting, Organization, and Function

2009 ◽  
pp. 247-263
Author(s):  
Smitha Babu Uthaman ◽  
Tanja Angela Godenschwege
2013 ◽  
Vol 373 (2) ◽  
pp. 244-257 ◽  
Author(s):  
Sonja J. McKeown ◽  
Adam S. Wallace ◽  
Richard B. Anderson

1998 ◽  
Vol 4 (S2) ◽  
pp. 1068-1069
Author(s):  
Ann-Marie Broome ◽  
Clarke F. Millette

Cell adhesion and cell adhesion molecules (CAMs) play a crucial role in testicular development and function. The seminiferous epithelium, the functional unit of the testis, represents a three dimensional architecture of supporting Sertoli cells (SC), and developing germ cells (GC). The seminiferous epithelium, therefore, must be receptive not only to individual cell growth and differentiation, but also to cell-cell interactions. Morphologically distinct cell-cell interactions occur between SC and GC and also between SC.[1] In general, these junctions can be categorized into three types: adhesive, occluding, and gap junctions. The orientation and function of these junctions are interaction dependent. For example, desmosome-like junctions (spot desmosomes) are found between SC and GC. These junctions are present in the basal and intermediate compartments of the testis and serve to translocate developing GC. SC-SC interactions, like the zonula occludens (tight junction), function as vectorial mediators, maintaining the blood-testis barrier and SC polarity.


2021 ◽  
Author(s):  
Shuwa Xu ◽  
Alina P Sergeeva ◽  
Phinikoula S. Katsamba ◽  
Seetha Mannepalli ◽  
Fabiana Bahna ◽  
...  

SUMMARYNeurons in the developing brain express many different cell adhesion molecules (CAMs) on their surfaces, and CAM interactions are essential for the determination of synaptic connectivity patterns. CAM binding affinities can vary by more than 200-fold, but the significance of affinity differences among CAMs is unknown. Here we provide a systematic characterization of the in vivo consequences of altering CAM affinity. Interactions between DIP-α and its binding partners Dpr6 and Dpr10 control synaptic targeting and cell survival for Drosophila optic lobe neurons. We generated mutations that change DIP-α::Dpr10 binding affinity and introduced these into the endogenous loci. We show that cell survival and synaptic targeting have different affinity requirements, and that there is a threshold affinity required for targeting. Reducing affinity causes graded loss-of-function phenotypes, while increasing affinity rescues cells that would normally die. Affinity reduction can be compensated for by increasing gene copy number.


1999 ◽  
Vol 106 (4) ◽  
pp. 467-476 ◽  
Author(s):  
Lilli Petruzzelli ◽  
Mimi Takami ◽  
H.David Humes

Sign in / Sign up

Export Citation Format

Share Document