Adaptation signal

Oleh :

Noni Mardian Trizana (G84050132) Dyta Hismayanti () Aditya Ardi Nugraha () R Haryo Bimo Setiarto () Bianca ()

Receptor Role in Adaptations

Insect B. thuringiensis Relationship B thuringienis is specific pathogen for insects and neatodes Bacteria Produces a spore and toxin crystal Cycle resembles anthrax Eat spores bacteria turns cow or other animal into more spores Insect eat spores and toxin, gut ruptures Bacteria turn caterpillars into more spores Insects - dead ones hang on leaves and spread spores to more insects

Receptors in Adaptations
Toxin Mechanism Cleaved by gut protease Binds a receptor Changes conformation Inserts into membrane and forms a pore Practical Uses Insecticide organic gardening either toxin or the bacteria Toxins are used in trangenic plants to fight insects

Receptors in Adaptation
Insect Adaptation The receptor for the toxin that causes the insect gut to rupture can be RNAi treated RNAi or RNA interference - is a cellular mechanism for the targeted destruction of RNA molecules RNAi can dramatically and selectively reduce the expression of an individual protein or receptor The receptor no longer allows for toxin binding and insects become resistant

Receptors that lead to disease resistance in humans

Malaria CCR2 expression P.vivax

(malaria causing strain) does not infect people candidate for vaccine HIV CCR5 not present then HIV resistance results CFTR receptor for Salmonella strains

Hormone Receptors
Most hormones circulate in blood and come

into contact with all cells. However only those cells with the correct receptor (the target cells) will respond

Types of Signaling
Autocrine: The hormone feeds-back on the cell of origin, without entering

blood circulation. Paracrine: The hormone diffuses to its target cells through extracellular space to neighbour cells.

Types of Signaling
Endocrine: The

classical mode where the hormones are delivered to target cells by blood.

 Brightness adaption

Merupakan fenomena penyesuaian mata manusia dalam membedakan gradasi tingkat kecemerlangan; Batas daerah tingkat kecemerlangan yang mampu dibedakan secara sekaligus oleh mata manusia lebih kecil dibandingkan dengan daerah tingkat kecemerlangan sebenarnya.

 Brightness Adaptation Human Visual System (HVS) dapat menampilkan

intensitas dengan range yg besar (1010) Tetapi secara simultan menerima intensitas dalam range yg jauh lebih kecil. Jika seseorang berada pada intensitas Ba (outside) dan masuk ke ruangan gelap, dia hanya dapat melihat hingga intensitas Bb. Mata membutuhkan waktu yg lebih lama untuk proses adaptasi dalam mencapai scotopic vision.

In ocular physiology, adaptation is the ability of the eye to adjust to various levels of darkness and light. The merging of signals by virtue of the diffuse ganglion cells, as well as horizontal and amacrine cells, allow a cumulative effect. This means that area of stimulation varies inversely with the intensity, a strong stimulus over 100 rods or less is equivalent to one that is weak and over 1,000 rods. In sufficiently bright light, convergence is low, but during dark adaptation, convergence of rod signals boost. This is not due to structural changes, but by a possible shutdown of inhibition that stops convergence of messages in bright light. If only one eye is open, the closed eye must adapt separately upon reopening to match the already adapted eye. Rods and cones in the eye are used during dark adaptation. Rods are more sensitive to light and so take longer to fully adapt to the change in light. Rod adaptation can take up to a few hours to completely regenerate. Cones take approximately 9 minutes to adapt to the dark.

Neural adaptation or sensory adaptation is a change over time in the responsiveness of the sensory system to a constant stimulus. It is usually experienced as a change in the stimulus. For example, if one rests one's hand on a table, one immediately feels the table's surface on one's skin. Within a few seconds, however, one ceases to feel the table's surface. The sensory neurons stimulated by the table's surface respond immediately, but then respond less and less until they may not respond at all; this is neural adaptation. More generally, neural adaptation refers to a temporary change of the neural response to a stimulus as the result of preceding stimulation. It is usually distinguished from memory, which is thought to involve a more permanent change in neural responsiveness. Some people use adaptation as an umbrella term that encompasses the neural correlates of priming and habituation. In most cases, adaptation results in a response decrease, but response facilitation does also occur. Adaptation is considered to be the cause of perceptual phenomena like afterimages and the motion aftereffect. In the absence of fixational eye movements, visual perception may fade out or disappear due to neural adaptation [1]. (See Adaptation (eye).) While large mechanosensory neurons such as type I/group A will display adaptation, smaller type IV/group C nociceptive neurons do not. As a result, pain does not usually subside rapidly but persists for long periods of time; in contrast, one quickly stops receiving touch or other sensory information if surroundings remain constant

Rod cells adapt to varying levels of ambient light

-Rhodopsin kinase phosphorylates activated rhodopsin (up to 7 sites) -Phosphorylated rhodopsin is less efficient in activating transducin -At high phosphorylation levels, arrestin binds rhodopsin and prevents binding of transducin

Cellular Adaptation Hypothesis

Cell deformation depends on cell siffness, K:

d(K) - dmin = Ddcell (K)

Mechanoreception also depends on cell stiffness:

Dt
low Kcell large d Kcell increases high Kcell small d

Cellular Adaptation Hypothesis

Cells may tune their stiffness to match the local

habitual loads Cellular Adaptation Cellular d - dmin = Ddcell Deformation DKcell

Cells may determine the tissue level strain set-point

Tissue Strains

Tissue Remodeling

by adapting to their mechanical environment

Variation on the theme G proteins can activate various effectors

second messengers used by GPCR signaling pathways

Some bacterial toxins irreversibly modify G proteins

Pertussis toxin ADP-ribosylates Gi and locks Gi in GDP (inactive) state; cannot exchange GDP for GTP