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Regarding light sensing in the retina; what is predicted tohappen if light activation of a GPCR occurs in the presence of anarrestin inhibitor?

Rhodopsin will not be phosphorylated by rhodopsin kinase

Rhodopsin will perpetually induce activation of cGMP gatedcation channels

Rhodopsin will perpetually induce cGMP breakdown

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Jarrod Robel
Jarrod RobelLv2
29 Sep 2019

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Exercise #5: The Nervous system and Perception

Task #1: Color vision


Introduction

In the human retina, there are two kinds of light-sensitive cells: rods and cones. These cells are located on the outside of the retina, away from the vitreous humor and against the choroid layer, and are covered by a later of bipolar and ganglion cells as well as neurons. Light enters the posterior chamber through the lens and must pass through several cell layers before it is absorbed by the rods and cones.

Cones are involved in color vision at daylight intensities. Generator potentials in a cone excite one neuron, giving high-level resolution vision. Cones will not cause neural firing at low light intensities and are, therefore, nonfunctional at night.

Rods provoke black-and-white vision at low light intensities. A bipolar cell associates with several rods, so that generator potentials sum in their effect. This assures neuronal firing at low light intensities and provides a highly sensitive vision but with less resolution.

Receptor convergence. A ganglion cell, which receives input from a number of rods, spread out over the retina, cannot pinpoint the source of a light stimulus as well as a ganglion cell, which is stimulated by a single photoreceptor. In the case of a ganglion cell receiving the added input of several rods, light hitting any one of the rods can cause a neural spike in the ganglion cell, but the brain has no way to know which rod was excited. It is therefore harder to pinpoint the location of light stimuli on the retina when the stimulus is detected by rods (as compared to cones). The result is that our ability to see detail, or our resolving power, is considerably lower under dim light conditions than under bright light conditions.

Dark adaptation. If you go from a lighted area to a very dark room, you will not be able to see. After about ten minutes, however, you begin to be able to see again. This occurs because the rhodopsin pigment, which gets broken down when it absorbs light, is continually re-synthesized in the rods. When there is very little light, very little rhodopsin gets broken down and the amount of rhodopsin gradually builds up, making the rod much more sensitive to dim light.

When light strikes a receptor cell, it triggers a photo-chemical reaction that leads to neuronal firing. If a rod or cone receives high-intensity light, the visual pigments will be temporarily bleached and will not absorb any more light. Within a matter of a few seconds, enzyme systems in the cells will restore the visual pigment to its light-absorbing form. This can be easily demonstrated. If, after viewing a bright light, the eye is quickly shut or turned to a dark wall, the bright image will persist as a positive afterimage because the high generator potential causes the continued firing of neurons. If the eye is cast on a lighter background after a few seconds, a negative afterimage, or a dark image of the object will appear. This is because the still bleached cells are not receptive to the light coming from the light background.

According to the Young-Helmholtz theory of color vision, there are three types of cone cells, which respond respectively to red, green, and blue light.

All other colors are perceived as the brain interprets impulses coming from a mix of these receptors. If an object of one color is viewed for a long period of time at high light intensity, the cones for that color will become bleached. The afterimage of the object will be seen in the complementary color.

The Exercise 6 PowerPoint will demonstrate afterimages to you. Use the slide show option to project the square of red light on your entire screen in a dark room. After staring intensely at the square for 30 seconds or so, without shifting your gaze, click enter to change the slide to a soft white. Continue staring at the screen as the change is made. What do you see? What was the color of the afterimage?

Repeat this experiment using a blue square. Before doing the experiment, hypothesize what color the afterimage will be according to the Young-Helmholtz theory.

Hypothesis to be tested: (2 pts)

What did you see when the experiment was conducted? (2 pts)

Was you hypotheses accepted or rejected? (1 pt)

Explain the colors seen in these afterimages using the Young-Helmholtz theory. (5 pts)

The binding of platelet derived growth factor (PDGF) to the PDGF receptor stimulates phosphorylation of 8 tyrosines in the receptor's cytoplasmic domain. The enzyme phosphatidylinositol 3'kinase (PI 3-kinase) binds to one or more of the phophotyrosines through its SH2 domains and is thereby activated. To identify the activation phosphotyrosines, you synthesize 8 pentapetides that contain the critical tyrosines (at the N-terninus) in their phosphorylated or unphosphorylated forms. You then mix an excess of each of the various pentapeptides with phosphorylated PDGF receptor and PI 3-kinase. Immunoprecipitation of the PDGF receptor will bring down any bound PI 3-kinase, which can be assayed by its ability to add 32P-phosphate to its substrate.

A) Draw a flow diagram showing how this assay works.

B) Do your results support the notion that PI-kinase binds to phosphotyrosines in the activated PDGF receptor? Why or why not?

C) THe amino acid sequences of the PDGF receptor pentapeptide tested above (number accodingly to the position of tyrosine in the PDGF receptor) and peptide segments that are known to bind to PI 3-kinase in other activated receptors are shown below. Which amino acid residues are most important and why?

684 YSNAL YMMMR (FGF receptor)

708 YMDMS YTHMN (insulin receptor)

719 YVPML YEVML (hepatocyte growth factor receptor)

731 YADIE YMDMK (steel factor receptor)

739 YMAPY YVEMR (CSF-1 receptor)

743 YDNYE

746 YEPSA

755 YRATL

Synergism in transcriptional regulation occurs when two transcription factors have a much greater effect when they are both active than would be predicted if one added their individual effects.
A. True
B. False

The N-terminal region of histones extends from nucleosomes. These histone tails can be covalently modified to signal that a gene in the region should be transcribed. What is the covalent modification?
A. Adding a poly A tail
B. Adding acetyl groups
C. Removing acetyl groups
D. Removing a poly A tail

You are studying how the estrogen receptor regulates expression of a particular gene in breast cancer cells grown in a test tube. You examine cells grown in the presence of estrogenic hormones. Using various biochemical techniques, you find that the activated estrogen receptor [i.e., with hormone(s) bound] binds to cis regulatory sequences in the gene of interest and recruits (physically interacts with) a protein that has histone deacetylase activity. Based on this information, do you predict that estrogen hormones induce transcription, have no effect on transcription, or suppress transcription of the target gene?
A. No effect
B. Induce
C. Suppress

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