**1. Introduction**

Vultures may have one of the strongest immune systems of all vertebrates (Apanius et al., 1983; Ohishi et al., 1979). Vultures are unique vertebrates able to efficiently utilize carcass from other animals as a food resource. These carrion birds are in permanent contact with numerous pathogens and toxins found in its food. In addition, vultures tend to feed in large groups, because carcasses are patchy in space and time, and feeding often incurs fighting and wounding, exposing vultures to the penetration of microorganisms present in the carri‐ on (Houston & Cooper, 1975). When an animal dies, the carcass provides the growth condi‐ tions necessary for many pathogens to thrive and produce high levels of toxins. Vultures are able to feed upon such a carcasses with no apparent ill effects. Therefore, vultures were pre‐ dicted to have evolved immune mechanisms to cope with a high risk of infection with viru‐ lent parasites.

Despite the potential interest in carrion bird immune system, little is known about the mo‐ lecular mechanisms involved in the regulation of this process in vultures. The aim of this chapter was to explore the genes from the griffon vulture (*Gyps fulvus*) leukocytes, particu‐ larly to search novel receptors, such as the toll-like receptor (TLRs) and other components involved in the immune sensing of pathogens and in the mechanism by which vulture are protected against toxins. This study is, to the best of our knowledge, the first report of ex‐ ploring the transcriptome in this interesting specie.

The toll-like receptor (TLR) family is an ancient pattern recognition receptor family, con‐ served from insects to mammals. Members of the TLR family are vital to immune func‐ tion through the sensing of pathogenic agents and initiation of an appropriate immune

© 2013 Mateos-Hernández et al.; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 Mateos-Hernández et al.; licensee InTech. This is a paper distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

response. The rapid identification of Toll orthologues in invertebrates and mammals sug‐ gests that these genes must be present in other vertebrates (Takeda, 2005). During the re‐ cent years, members of the multigene family of TLRs have been recognised as key players in the recognition of microbes during host defence (Hopkinsn & Sriskandan, 2005). Recognition of pathogens by immune receptors leads to activation of macrophag‐ es, dendritic cells, and lymphocytes. Signals are then communicated to enhance expres‐ sion of target molecules such as cytokines and adhesion molecules, depending on activation of various inducible transcription factors, among which the family NF-kappaB transcription factors plays a critical role. The involvement of nuclear factor-kappa B (NFκB) in the expression of numerous cytokines and adhesion molecules has supported its role as an evolutionarily conserved coordinating element in organism's response to situa‐ tions of infection, stress, and injury. In many species, pathogen recognition, whether mediated via the Toll-like receptors or via the antigen-specific T- and B-cell receptors, in‐ itiates the activation of distinct signal transduction pathways that activate NF-κB (Ghosh et al., 1998). TLR-mediated NF-κB activation is also an evolutionarily conserved event that occurs in phylogenetically distinct species ranging from insects to mammals.

**ORF /Acs number Function Assignment<sup>1</sup>**

associated effects involving normal growth and cancer proliferation.

class I genes and activates those genes. Acts as a tumor suppressor.

exocytosis. This protein regulates phospholipase A2 activity.

providing the energy for active transport of various nutrients.

60S ribosomal Binds to a specific region on the 26S rRNA RP

Glycolytic enzyme, also PGK-1 may acts as a polymerase alpha cofactor protein (primer

Identification of Key Molecules Involved in the Protection of Vultures Against Pathogens and Toxins

Potential transcription factor. May mediate some of the neuroprotective peptide VIP-

Tumor suppressor. It blocks the growth, invasion, and metastatic properties of mammary

Activator of LATS1/2 in the Hippo signaling pathway which plays a pivotal role in organ size control and tumor suppression by restricting proliferation and promoting apoptosis.

May cooperate with CD180 and TLR4 to mediate the innate immune response to bacterial lipopolysaccharide (LPS) and cytokine production. Important for efficient CD180 cell surface

Chemotactic factor that attracts neutrophils, basophils, and T-cells, but not monocytes. It is also involved in neutrophil activation. It is released from several cell types in response to an

May participate in mRNA transport in the cytoplasm. Critical component of the oxidative

Specifically binds to the upstream regulatory region of type I IFN and IFN-inducible MHC

Calcium/phospholipid-binding protein which promotes membrane fusion and is involved in

Enzyme regulation: Plasma membrane-associated small GTPase which cycles between an active GTP-bound and inactive GDP-bound state. In active state binds to a variety of effector proteins to regulate cellular responses, such as secretory processes, phagocytose of apoptotic cells and epithelial cell polarization. Augments the production of reactive oxygen species

Transcriptional activator. Binds the cAMP response element (CRE), a sequence present in

This protein promotes the GTP-dependent binding of aminoacyl-tRNA to the A-site of

Catalytic activity: Catalytic component of the active enzyme, which catalyzes the hydrolysis of ATP coupled with the exchange of sodium and potassium ions across the plasma membrane. This action creates the electrochemical gradient of sodium and potassium ions,

DNA repair enzyme that can remove a variety of covalent adducts from DNA through hydrolysis of a 5'-phosphodiester bond, giving rise to DNA with a free 5' phosphate.

Important for the balance of metabolites in the pentose-phosphate pathway. CA

Polynucleotide 5'-kinase involved in rRNA processing. RP

Cytokine that is chemotactic for monocytes but not for neutrophils. Binds to CCR8 IS

May play a role during erythropoiesis through regulation of transcription factor DDIT3. OT

CA

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http://dx.doi.org/10.5772/54191

RP

RP

OT

IS

IS

OT

IS

RP

IS

RP

OT

CA

OT

Phosphogycerato kinase 1 PGK1 JX889400

Activity-dependent neuroprotector homeobox (ADNP) JX889402

Serpin B5-like JX889399

40S ribosomal protein S3a JX889382

Mps one binder kinase activatorlike 1B, JX889412

Lymphocyte antigen 86 [LY86] JX889396

Constitutive coactivator of PPAR-gamma-like protein 1, JX889388

Interferon regulatory factor 1 (IRF-1), JX889416

Annexin A1 [ANXA1], JX889410

Chemokine (C-C motif) ligand 1, JX889398

Ras-related C3 botulinum toxin substrate 2 (RAC2) JX889392

Activating transcription factor 4 (ATF4), JX889393

Elongation factor 1 alpha 1 (EF-1 alpha-1), JX889383

Polynucleotide 5' hydroxyl-kinase NOL9, JX889408

Sodium/potassium -transporting ATPase subunit alpha-1, JX889386

Tyrosyl-DNA phosphodiesterase 2 (TDP2), JX889415

Transaldolase (EC 2.2.1.2) [TALDO1] JX889384

IL-8 JX889394 recognition protein).

tumors.

expression.

inflammatory stimulus.

(ROS) by NADPH oxidase

many viral and cellular promoters.

ribosomes during protein biosynthesis

stress-induced survival signaling.

Botulinun toxins are the most deadly neurotoxins known to man and animals. When an animal dies from botulism or other causes, the carcass provides the growth conditions necessary for *C. botulinun* to thrive and produce high levels of toxins. Certain species of carrion-eater birds and mammals are able to feed upon such carcasses with no apparent ill effects. Turkey vultures (*Cathartes aura*), have been shown to be highly resistant to bot‐ ulinun toxins (Kalmbach, 1993; Pates, 1967, cited by Oishi et al., 1979). The mechanism by which these species are protected against botulinun toxin was investigated by explor‐ ing the genes from the griffon vulture (*Gyps fulvus*) leukocytes, particularly with the identification of ORFs with homology to the Ras-related botulinun toxin substrate 2 (RAC2), ADP-ribosylation factor 1 (a GTP-binding protein that functions as an allosteric activator of the cholera toxin catalytic subunit); a ras-related protein Rabb-11-B-like, and other ORFs with homology to some chemical mediators, such as IL-8, Chemokine (C-C motif) ligand 1.
