Analysis of GPCR Activity on the EIDAQ™ 100 High Throughput Microscopy System 

This application note describes the successful deployment of the NORAK Transfluor™ assay for GPCR

activity on the EIDAQ™ 100 High Throughput Microscopy system from Q3DM. The Norak Transfluor™

assay measures GPCR activation by the formation of GFP labeled pits, or vesicles, depending on the

GPCR that is being expressed by a cell. The EIDAQ™ 100 is a novel High Throughput Microscopy

(HTM) system that delivers accurate, quantitative, imaging, and analysis of cell populations, at high

speeds, directly from microtiter plates. For accurate reading/measurement, the EIDAQ™ 100 quantifies

distribution of fluorescence emanating from the GPCR associated arrestin-GFP fusion protein and in

sub-cellular compartments. Definitive measurements are quantified with a proprietary, multi-scale

vesicle definition algorithm developed at Q3DM.


Background and Significance

GPCRs mediate the activity of cell surface receptors and the transduction of a myriad of intra-cellular

responses. GPCRs have proven to be a highly amenable class of targets for successful therapeutic

intervention. In fact, of the approximately 500 drugs currently on the market today, more than 30% are

mediated through the activation of GPCRs. Because GPCRs are membrane-bound proteins, they have

been difficult to study in cell extracts, or to isolate and characterize. To directly ascertain GPCR activity,

intact cell-based assays are quickly becoming a method of choice in high-throughput screening.

GPCRs transduce extracellular signals through the formation of protein complexes that effect both

activation and subsequent desensitization of a cell surface receptor. Agonist binding to a receptor at the

cell surface initiates a conformational change in the intracellular domain of the receptor that results in the

phosphorylation of the receptor and subsequent binding of arrestin to the receptor. The arrestin-receptor

complex is then transported to clathrin-coated pits and internalized to clathrin-coated vesicles. Finally,

the entire complex is delivered to the endosomes. Some GPCRs dissociate from arrestin at or near the

plasma membrane, while others remain associated and traffic into endocytic vesicles.

Norak Transfluor™ GPCR Assay – Q3DM EIDAQ100™ HTM Analysis 


This validation report describes the performance of the NORAK Transfluor™ assay for GPCR

activity on the EIDAQ™ 100 High Throughput Microscopy (HTM) system from Q3DM. The

EIDAQ™ 100 HTM system performs accurate reading & measurement of GPCR activity by

quantification of GPCR associated formation of GFP labeled pits or vesicles using a

proprietary, multi-scale vesicle definition algorithm. The performance of this algorithm in

combination with the EIDAQ™ 100 HTM system was evaluated by repeatably determining EC50

& IC50 values for agonist and antagonist well plates. The results showed very good repeatability

of the GPCR analysis using the EIDAQ™ 100 HTM system and CytoShop™ software suite with

the proprietary GPCR algorithm proving that the Q3DM system in combination with the Norak

Transfluor™ assay presents a powerful quantification tool for GPCR activity.

Background and Significance

GPCRs mediate the activity of cell surface receptors and the transduction of a myriad of intracellular responses. They have proven to be a highly amenable class of targets for successful

therapeutic intervention. In fact, of the approximately 500 drugs currently on the market today,

more than 30% are mediated through the activation of GPCRs. Because GPCRs are membranebound proteins, they have been difficult to study in cell extracts, or to isolate and characterize.

To directly ascertain GPCR activity, intact cell-based assays are quickly becoming a method of

choice in high-throughput screening.

GPCRs transduce extracellular signals through the formation of protein complexes that effect

both activation and subsequent desensitization of a cell surface receptor. Agonist binding to a

receptor at the cell surface initiates a conformational change in the intracellular domain of the

receptor that results in the phosphorylation of the receptor and subsequent binding of arrestin to

the receptor. The arrestin-receptor complex is then transported to clathrin-coated pits and

internalized to clathrin-coated vesicles. Finally, the entire complex is delivered to the

endosomes. Some GPCRs dissociate from arrestin at or near the plasma membrane, while others

remain associated and traffic into endocytic vesicles.

The combination of automated sub-micron imaging, proprietary image processing and the Norak

Transfluor™ assay enables accurate measurement of GPCR activity through vesicle response

and pit formation. Validated results of GPCR activity using the EIDAQTM 100 HTM system are

presented with fluorescent images and dose response curves.

Experimental Methods

Norak Transfluor™ Assay Plates

In the Norak Transfluor™ assay, a cell line is developed to monitor the interaction of a given

GPCR and a GFP fused to ß-arrestin. When each GPCR is activated, the ß-arrestin will bind to

the membrane associated GPCR. The activated ß-arrestin-GPCR complex then enters clathrincoated pits and migrates to intracellular vesicles via the endosomal pathway. Some GPCRs retain

the arrestin molecule throughout this process, so that vesicles will fluoresce with GFP. Other

GPCRs will dissociate from the arrestin such that the GFP remains with the pits, or is released to

the intracellular space, and the receptors recycle back to the cell surface and bind arrestin again.

VALIDATION REPORT

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www.q3dm.com

Negative

Positive

Figure 1: Cell analysis for GPCR - example

images from a well plate scan; negative response

(top) compared to positive response (bottom);

pseudo-color overlay of nuclear dye Hoechst

(blue) and GFP ß-arrestin (green) shown in left

column, additionally masks for GPCR

measurement (red) shown in right column.

Two different plates were used, one containing a wild type cell line, the other containing an

enhanced cell line. The layout of the plates was identical and is shown in Table 1.