Goosecoid
There are two goosecoid genes in the chick, GSX and GSC. The two homeodomains are 74% identical. In the first few hours of chick embryogenesis, the expression pattern of GSX is similar to that of GSC, in the posterior margin of the embryo and the young primitive streak. GSX transcripts are already detectable before primitive streak formation and gastrulation when the hypoblast sheet expands. Expression is seen as a crescent associated with Koller's sickle at the posterior margin of the blastoderm. The majority of GSX-positive cells are located in the epiblast. The deep layer of the posterior epiblast, the location of presumptive primitive streak cells, shows a weak staining for GSX. When the streak has progressed to its maximal length, GSX transcripts become less abundant in the primitive streak itself, with expression remaining in the primitive ridges, surrounding the streak. The primitive groove and the primitive pit, major sites of avian gastrulation, are negative for GSX expression. The more posterior GSX-positive part of the primitive streak induces gastrulation, while the more anterior GSC-expressing part induces neurulation. At this stage, a new domain arises around the anterior third of the primitive streak, with expressing cells in the epiblast surrounding Hensen's node in a circular and later pear-shaped expression. The limits of GSX expression reveal a sharp boundary between the strongly stained central neuroectodermal region and the unstained more peripheral epiblast (presumptive epidermis). Fate mapping studies have identified this domain as the early neural plate. GSC is expressed in the anterior part of the primitive streak, then in the node, and finally in the precordal plate. After full extention of the streak, the fate of the cells now characterized by GSX is to undergo neurulation, while those expressing GSC undergo gastrulation (Lemaire, 1997).
Different types of endoderm, including primitive, definitive and mesendoderm, play a role in the
induction and patterning of the vertebrate head. These three types of endoderm are defined in order to compare the mechanism of head induction in model vertebrate organisms. (1) The primitive endoderm is a prospective extraembryonic tissue present in the mouse and the chick, whereas amphibia generate no extraembryonic tissue at all. This endoderm is not a product of gastrulation, and its fate is to become the stalk of the yolk sac. (2) The definitive anterior endoderm develops into the foregut and the liver. In amphibia, it also comprises yolky cells outside the epithelial lining. (3) The precordal mesendoderm as an organizer-derived tissue migrates anteriorly to lie under the developing forebrain. The formation of the anterior neural
plate has been studied in chick embryos using the homeobox gene GANF as a marker. GANF is a member of the 'Anf' (anterior neural folds) family, from which a single member has been found in vertebrates, such as fish (Danf), amphibia (Xanf), chick (GANF), mice (Hesx1/Rpx) and human (HANF/HESX1), but has not been found in Drosophila. GANF is first expressed after
mesendoderm ingression from Hensen's node. After transplantation, neither the avian
hypoblast nor the anterior definitive endoderm is capable of GANF induction, whereas the
mesendoderm (young head process, prechordal plate) exhibits a strong inductive potential. GANF
induction cannot be separated from the formation of a proper neural plate, which requires an intact
lower layer and the presence of the prechordal mesendoderm. It is inhibited by BMP4 and promoted
by the presence of the BMP antagonist Noggin. In order to investigate the inductive potential of the
mammalian visceral endoderm, use was made of rabbit embryos which, in contrast to mouse embryos, allow the
morphological recognition of the prospective anterior pole in the living, pre-primitive-streak embryo.
The anterior visceral endoderm from such rabbit embryos induces neuralization and independent,
ectopic GANF expression domains in the area pellucida or the area opaca of chick hosts. In terms of the timing and the location of the head organizer, the chick is more similar to the frog, where the signaling comes from the organizer and its derivative, the mesendoderm. In contrast, head-inducing signals in mammals originate from the anterior visceral endoderm. Hence, mouse embryos begin the patterning of the head long before the mesendoderm ingresses, whereas chick head development occurs only after endoderm formation. Only mammals have shifted the head-inducing signals into the primitive endoderm, and they begin the induction and patterning process of the head long before (about 24 hours in mice and rabbits) the mesendoderm ingresses. Several genes are expressed in the independent primitive endoderm domain (the anterior visceral endoderm) in the mammalian head organizer before or at the onset of primitive streak formation, prior to their expression in the axial mesendoderm or the node during gastrulation. These include the homeobox genes Hesx1 (Rpx), Goosecoid, Lim1, Hex and Otx2; the forkhead gene HNF3beta; the nuclear protein gene mrg1; the growth factor gene Nodal, and the antigen VE-1. Thus, the
signals for head induction reside in the anterior visceral endoderm of mammals whereas, in birds and
amphibia, they reside in the prechordal mesendoderm, indicating a heterochronic shift of the head
inductive capacity during the evolution of mammalia (Knoetgen, 1999).
The common beginning and later segregation of both gene activities during ontogeny could indicate a similar dynamic during phylogeny. This assumption is strengthened by findings concerning the Drosophila goosecoid gene. The primary structure of the Drosophila homeodomain is equidistant from the two homeodomains of the chick (73.7%). The fly gene is expressed only in ectodermal structures, the brain anlage and the esophagus, and its derivative, the stomatogastric nervous system; mutants have defects in neural development (Hahn, 1996). It is suggested that the basic goosecoid information was split into two genes during the evolution of chordates, allowing the generation of novel fates and inductive potentials. It is speculated that gastrulation of goosecoid cells only became possible when, at the same time, a second goosecoid identity could be maintained in the ectoderm. As a consequence, a simple sequence, going from endoderm to notochord, was converted to a more elaborate system of endoderm-mesoderm-notochord. The two lower groups of chordates, ascidians (phylum Urochordata) and Amphioxus (phylum Cephalochordata within the phylum Chordata) indeed lack a prechordal mesendoderm, and their notochord is formed in continuity with the endoderm during gastrulation. A direct consequence of a prechordal plate in vertebrates is the more complex organization of the forebrain, as evident by the presence of a unique ventral forebrain. In the chick, the nervous system develops from GSX cells which are induced and patterned under the influence of GSC cells. This interaction is exerted in a planar fashion, while still in the anterior streak, and vertically after gastrulation from the prechordal plate (Lemaire, 1997).
The homeobox-containing gene goosecoid (gsc) has been implicated in a variety of embryonic
processes from gastrulation to rib patterning. The role it plays during chick limb
development has been analyzed. Expression is initially observed at stage 20 in a proximal-anterior-ventral (pav) domain of the
early limb bud that expands during subsequent stages. Later in limb development a second domain of
expression appears distally that resolves to regions surrounding the condensing cartilage. In order
to understand the function of gsc in limb development, the effect of misexpressing
gsc throughout the limb has been examined. Two striking phenotypes are observed. The first, evident at stage 24, is an
alteration in the angle of femur outgrowth from the main body axis. The second, which can be detected
at day 10 of development, is an overall decrease in the size of the limb, with bones that are small,
misshapen and bent. These phenotypes correlate with a decrease in levels of Hox gene expression in
gsc-infected limb buds. From these results it is suggested that gsc may normally function to regulate
growth and patterning of the limb, perhaps through regulation of Hox gene expression. The pav expression of gsc may contribute to the absence of Hoxd gene expression in that region and thereby affect the early patterning of the limb and in particular the limb articulation. Examination of the phenotype of gsc mutants suggests a role for gsc in patterning cartilage elements in the developing limb, in particular affecting the articulation of the hip and growth of the femur (Heanue, 1997).
Initially
suggested to be involved in organizing the embryo during early development, Goosecoid has since
been demonstrated to be expressed during organogenesis, most notably in the head, the limbs and
the ventrolateral body wall. Mice
that are homozygous for the Goosecoid mutation do not display a gastrulation phenotype and are
born, but they do not survive more than 24 hours. Analysis of the homozygotes reveals
numerous developmental defects affecting those structures in which Goosecoid is expressed during
its second (late) phase of embryonic expression. Predominantly, these defects involve the lower
mandible and its associated musculature including the tongue, the nasal cavity and the nasal pits, as
well as the components of the inner ear (malleus, tympanic ring) and the external auditory meatus.
Although the observed phenotype is in accordance with the late expression domains of goosecoid in
wild-type embryos, the lack of an earlier phenotype is probably the result of functional
compensation by other genes (Yamada, 1995).
Gsc-1 expression marks cells with Spemann organizer, or axis-inducing, activity in the vertebrate gastrula. Gsc-1 knockouts, however, did not display phenotypes related to the early phase of expression. In this paper, additional phenotypes for the Gsc-1 mouse mutant are presented. Examination of the base of the cranium in the dorsal view reveals fusions and deletions in the midline of the prechordal chondrocranium. These defects were correlated with the sites of expression of Gsc-1 in the prechordal plate/foregut endoderm in the day 7.5/8.5 embryo. Althought the skeletal structures involved are derived from neural crest, they develop in close association with Gsc-1-expressing cells in the prechordal plate during early development. The notochord does not express Gsc-1 at these stages. Gsc-1 expression in proximal limb buds is correlated with malformations of the shoulder and hip articulations. In addition, ribs in the seventh cervical vertebra were observed with low penetrance. The role of Gsc-1 during gastrulation and axial development is discussed in relation to possible compensatory interactions with other genes such as HNF-3beta and the recently identified Gsc-2 and
Gsc-3 genes (Belo, 1998).
The homeobox gene goosecoid and the winged-helix gene Hepatic Nuclear Factor-3ß
(Drosophila homolog Forkhead) are co-expressed in all three germ layers in the anterior primitive streak and at the rostral
end of mouse embryos during gastrulation. In the early mid-streak stage, gsc expression is encompased within the domain of expression of HNF-3ß, while HNF-3ß is expressed by itself in the ectoderm germ layer, in particular in the distal-most region of the primitive streak. Since the two genes are coexpressed, a test was made as to whether they interact. Double-mutant embryos of genotype gsc (-/-);HNF-3ß(+/-) show a
new phenotype as early as embryonic days 8.75. There is a dramatic reduction in forebrain size, abnormal branchial arches and defects in heart looping. Analysis of D-V molecular markers demonstrate that dorsal cell fates are expanded ventrally, while ventral cell fates, including optic vesicles in the diencephalon and floor plate cells in the midbrain and hindbrain, are missing in severely affected individuals. Loss of Sonic hedgehog and HNF-3ß
expression is observed in the notochord and ventral neural tube of these embryos. These results
indicate that gsc and HNF-3ß interact to regulate Shh expression and consequently dorsal-ventral
patterning in the neural tube. In the forebrain of the mutant embryos, severe growth defects and
absence of optic vesicles could involve loss of expression of fibroblast growth factor-8, in addition to
Shh. These results also suggest that interaction between gsc and HNF-3ß regulate other signaling
molecules required for proper development of the foregut, branchial arches and heart (Filosa, 1997).
Goosecoid (gsc) is expressed in the organizer region of vertebrate embryos undergoing the movements of gastrulation.
Likewise, the early heart tube (8.5-9.5 dpc) undergoes a similar process of looping to bring the atrial region cranial and dorsal
to the ventricular region, eventually giving rise to the four chambered heart. In order to determine whether gsc is similarly
involved in heart morphogenesis, in situ hybridization and RT-PCR were used to detect gsc expression in the embryonic mouse
heart. gsc mRNA is expressed in the developing mouse heart, and is localized to the
sites that divide the primitive heart tube into a four chambered heart (Conway, 1999).
Ptx1 (see Drosophila Ptx1) is a member of the small bicoid family of homeobox-containing genes; it was isolated as a
tissue-restricted transcription factor of the pro-opiomelanocortin gene. The homeodomain of Ptx1 contains a lysine at position 9 of the recognition helix (position 60 of the homeodomain). This residue is strategically placed in the major groove of DNA and it is a major determinant of DNA-binding specificity recognizing the CC doublet of the target site. This lysine residue defines the bicoid subfamily of homeoboxes, including Otx1 and 2 and Goosecoid. Ptx1 expression during mouse and
chick embryogenesis was determined by in situ hybridization in order to delineate its putative role in
development. In the head, Ptx1 expression is first detected in the ectoderm-derived stomodeal
epithelium at E8.0. Initially, expression is only present in the stomodeum and in a few cells of the
rostroventral foregut endoderm. A day later, Ptx1 mRNA is detected in the epithelium and in a streak
of mesenchyme of the first branchial arch, but not in other arches. Ptx1 expression is maintained in all
derivatives of these structures, including the epithelia of the tongue, palate, teeth and olfactory system,
and in Rathke's pouch. Expression of Ptx1 in craniofacial structures is strikingly complementary to the
pattern of goosecoid expression. Gsc labelling in the mandibular component is confined to a central stripe of mesenchyme whereas Ptx1 labelling is observed more laterally.
Similarly, the epithelium of the first arch, a site of strong Ptx1 expression, is not labelled by the Gsc probe. Ptx1 is expressed early (E6.8) in posterior and
extraembryonic mesoderm, and in structures that derive from these. The restriction of expression to
the posterior lateral plate is later evidenced by exclusive labelling of the hindlimb but not forelimb
mesenchyme. In the anterior domain of expression, the stomodeum is shown by fate mapping to
derive from the anterior neural ridge (ANR) which represents the most anterior domain of the embryo.
The concordance between these fate maps and the stomodeal pattern of Ptx1 expression supports the
hypothesis that Ptx1 defines a stomodeal ectomere that lies anterior to the neuromeres that have
been suggested to constitute units of a segmented plan directing head formation. Drosophila Gsc is expressed in the stomodeal invagination, while vertebrate Gsc is not. Based on these gene expression patterns, it is thought that the vertebrate stomodeum is an evolutionary innovation, assuring the ventral placement of the mouth (Lanctot, 1997).
Mice homozygous for a targeted deletion of the homeobox
gene Goosecoid (Gsc) have multiple craniofacial defects. To
understand the mechanisms responsible for these defects,
the behavior of Gsc-null cells was examined in morula
aggregation chimeras. In these chimeras, Gsc-null cells
were marked with beta-galactosidase (beta-gal) activity using the
ROSA26 lacZ allele. In addition, mice with a lacZ gene that
had been introduced into the Gsc locus were used as a guide
to visualize the location of Gsc-expressing cells. In Gsc-null - wild-type chimeras, tissues that would normally not
express Gsc were composed of both Gsc-null and wild-type
cells that were well mixed, reflecting the overall genotypic
composition of the chimeras. However, craniofacial tissues
that would normally express Gsc were essentially devoid of
Gsc-null cells. Furthermore, the nasal capsules and
mandibles of the chimeras had defects similar to Gsc-null
mice. These vary in severity depending on the proportion
of Gsc-null cells. These results combined with the analysis
of Gsc-null mice suggest that Gsc functions cell
autonomously in mesenchyme-derived tissues of the head.
A developmental analysis of the tympanic ring bone, a bone
that is always absent in Gsc-null mice because of defects at
the cell condensation stage, shows that Gsc-null cells have
the capacity to form the tympanic ring condensation in the
presence of wild-type cells. However, analysis of the
tympanic ring bones of 18.5 d.p.c. chimeras suggests that
Gsc-null cells are not maintained. The participation of
Gsc-null cells in the tympanic ring condensation of
chimeras may be an epigenetic phenomenon that results in
a local environment in which more precursor cells are
present. Thus, the skeletal defects observed in Gsc-null
mice may reflect a regional reduction of precursor cells
during embryonic development (Rivera-Pérez, 1999).
The homeobox gene goosecoid was the first specific genetic marker of Spemann's organizer in vertebrate embryos to be discovered. In the frog, misexpression of
this gene by RNA injection produces duplication of the posterior axis. For these reasons, the recent finding that mice lacking goosecoid function have no early axial
defects was rather surprising. The neural inducing strength of wild-type and goosecoid-mutant mouse nodes was examined by transplantation into primitive streak
stage chick embryos. Wild-type mouse nodes strongly induce the neural-specific transcription factors Sox2 and Sox3 in the chick host. Homozygous goosecoid(-/-) nodes are severely impaired in their ability to induce both genes. Heterozygous goosecoid(+/-) nodes induce Sox3 as well as wild-type nodes, but resemble -/-
nodes in their limited ability to induce Sox2. It is proposed that goosecoid does play a role in regulating the neural inducing strength of the node and that regulative
mechanisms exist that mask the early phenotypic consequences of goosecoid mutations in the intact mouse embryo (Zhu, 1999).
A mammalian forkhead domain protein, FAST2, has been identifed that is required for induction of the goosecoid (gsc) promoter by
TGF beta or activin signaling. FAST2 binds to a sequence in the gsc promoter, but efficient transcriptional activation and
assembly of a DNA-binding complex of FAST2, Smad2, and Smad4 requires an adjacent Smad4 site. Smad3 is closely related
to Smad2 but suppresses activation of the gsc promoter. Inhibitory activity is conferred by the MH1 domain, which unlike that
of Smad2, binds to the Smad4 site. Through competition for this shared site, Smad3 may prevent transcription by altering the
conformation of the DNA-binding complex. Thus, a mechanism is described whereby Smad2 and Smad3 positively and
negatively regulate a TGF beta/activin target gene (Labbe, 1998).
Gscl, a paired-type homeobox gene, has been implicated in the pathology of DGS/VCFS
by virtue of its genomic location and its structural similarity to the Gsc gene family.
Immunohistochemical and in situ studies were performed to examine the expression
pattern of this gene during embryonic development. Both in situ and
antibody staining localizes GSCL expression to a cluster of cells in the pons region of the
developing brain. This GSCL expression pattern shows partial overlap with that of
Pax6. More detailed immunohistochemistry reveals the GSCL in primordial germ cells
during migration from the epithelium of the hindgut, as well as later in development as the germ cells colonize the
developing gonads. GSCL was not detected in tissues affected in DGS/VCSF (Galili, 1998).
The middle ear apparatus is composed of three endochondrial ossicles (the stapes, incus and malleus) and two membranous bones, the tympanic ring and the
gonium, all of which which act as structural components to anchor the ossicles to the
skull. Except for the stapes, these skeletal elements are unique to mammals
and are derived from the first and second branchial arches. In
combination with goosecoid (Gsc), the Bapx1 gene
defines the structural components of the murine middle ear. During embryogenesis, Bapx1 is expressed in a discrete domain
within the mandibular component of the first branchial arch and later in the primordia of middle ear-associated bones, the gonium and tympanic ring.
Consistent with the expression pattern of Bapx1, mouse embryos
deficient for Bapx1 lack a gonium and display hypoplasia of the
anterior end of the tympanic ring. At E10.5, expression of Bapx1
partially overlaps that of Gsc and although Gsc is required
for development of the entire tympanic ring, the role of Bapx1 is
restricted to the specification of the gonium and the anterior tympanic ring. Thus, simple overlapping expression of these two genes appears to account for the patterning of the elements that compose the structural components of the middle ear and suggests that they act in concert. In addition, Bapx1 is expressed both within and surrounding the
incus and the malleus. Examination of the malleus shows that the width, but
not the length, of this ossicle is decreased in the mutant mice. In
non-mammalian jawed vertebrates, the bones homologous to the mammalian middle ear ossicles compose the proximal jaw bones that form the jaw articulation (primary jaw joint). In fish, Bapx1 is responsible for the formation of the joint between the quadrate and articular (homologs of the malleus and incus, respectively) enabling an evolutionary comparison of the role of a regulatory gene in the transition of the proximal jawbones to middle ear ossicles. Contrary to expectations, murine Bapx1 does not affect the articulation of the malleus and incus. This change in role of Bapx1 following the transition to the mammalian ossicle configuration is not due to a change in expression pattern but results from an inability to regulate Gdf5 and Gdf6, two genes predicted to be essential in joint formation (Tucker, 2004).
Goosecoid (Gsc) is a homeodomain-containing transcription factor present in a wide variety of vertebrate species and known to regulate formation and patterning of embryos. In embryonic carcinoma P19 cells, the transcription factor TFII-I forms a complex with Smad2 upon transforming growth factor ß (TGFß)/activin stimulation, is recruited to the distal element (DE) of the Gsc promoter, and activates Gsc transcription. BEN is a member of the TFII-I family of transcription factors. TFII-I and BEN share multiple helix-loop-helix (HLH) domains and a leucine zipper domain. Despite the structural similarity, TFII-I often acts as a transcriptional activator, and BEN often acts as a transcriptional repressor. Downregulation of endogenous TFII-I by small inhibitory RNA in P19 cells abolishes the TGFß-mediated induction of Gsc. Similarly, Xenopus embryos with endogenous TFII-I expression downregulated by injection of TFII-I-specific antisense oligonucleotides exhibit decreased Gsc expression. Unlike TFII-I, the related factor BEN (binding factor for early enhancer) is constitutively recruited to the distal element in the absence of TGFß/activin signaling and is replaced by the TFII-I/Smad2 complex upon TGFß/activin stimulation. Overexpression of BEN in P19 cells represses the TGFß-mediated transcriptional activation of Gsc. These results suggest a model in which TFII-I family proteins have opposing effects in the regulation of the Gsc gene in response to a TGFß/activin signal (Ku, 2005).
Activator protein-1 (AP-1) is a mediator of BMP or FGF signaling during Xenopus embryogenesis. However, specific role of AP-1 in activin signaling has not been elucidated during vertebrate development. This study provides new evidence showing that overexpression of heterodimeric AP-1 comprised of c-jun and c-fos [AP-1(c-Jun/c-Fos)] induces the expression of BMP-antagonizing organizer genes (noggin, chordin and goosecoid) that were normally expressed by high dose of activin. AP-1(c-Jun/c-Fos) enhanced the promoter activities of organizer genes but reduced that of PV.1, a BMP4-response gene. A loss of function study clearly demonstrated that AP-1(c-Jun/c-Fos) is required for the activin-induced organizer and neural gene expression. Moreover, physical interaction of AP-1(c-Jun/c-Fos) and Smad3 cooperatively enhanced the transcriptional activity of goosecoid via direct binding on this promoter. Interestingly, Smad3 mutants at c-Jun binding site failed in regulation of organizer genes, indicating that these physical interactions are specifically necessary for the expression of organizer genes. In is concluded that AP-1(c-Jun/c-Fos) plays a specific role in organizer gene expression downstream of activin signal during early Xenopus embryogenesis (Lee, 2011).
How multiple developmental cues are integrated on cis-regulatory modules (CRMs) for cell fate decisions remains uncertain. The Spemann-Mangold organizer in Xenopus embryos expresses the transcription factors Lim1/Lhx1, Otx2, Mix1, Siamois (Sia) and VegT. Reporter analyses using sperm nuclear transplantation and DNA injection showed that cerberus (cer) and goosecoid (gsc) are activated by the aforementioned transcription factors through CRMs conserved between X. laevis and X. tropicalis. ChIP-qPCR analysis for the five transcription factors revealed that cer and gsc CRMs are initially bound by both Sia and VegT at the late blastula stage, and subsequently bound by all five factors at the gastrula stage. At the neurula stage, only binding of Lim1 and Otx2 to the gsc CRM, among others, persists, which corresponds to their co-expression in the prechordal plate. Based on these data, together with detailed expression pattern analysis, a new model of stepwise formation of the organizer is proposed, in which (1) maternal VegT and Wnt-induced Sia first bind to CRMs at the blastula stage; then (2) Nodal-inducible Lim1, Otx2, Mix1 and zygotic VegT are bound to CRMs in the dorsal endodermal and mesodermal regions where all these genes are co-expressed; and (3) these two regions are combined at the gastrula stage to form the organizer. Thus, the in vivo dynamics of multiple transcription factors highlight their roles in the initiation and maintenance of gene expression, and also reveal the stepwise integration of maternal, Nodal and Wnt signaling on CRMs of organizer genes to generate the organizer (Sudou, 2012).
Short stature, auditory canal atresia, mandibular hypoplasia, and skeletal abnormalities (SAMS) has been reported previously to be a rare, autosomal-recessive developmental disorder with other, unique rhizomelic skeletal anomalies. These include bilateral humeral hypoplasia, humeroscapular synostosis, pelvic abnormalities, and proximal defects of the femora. To identify the genetic basis of SAMS, molecular karyotyping and whole-exome sequencing (WES) were used to study small, unrelated families. Filtering of variants from the WES data included segregation analysis followed by comparison of in-house exomes. A homozygous 306 kb microdeletion and homozygous predicted null mutations were found of GSC, encoding Goosecoid homeobox protein, a paired-like homeodomain transcription factor. This confirms that SAMS is a human malformation syndrome resulting from GSC mutations. Previously, Goosecoid has been shown to be a determinant at the Xenopus gastrula organizer region and a segment-polarity determinant in Drosophila. Data is presented in this study on Goosecoid protein localization in staged mouse embryos. These data and the SAMS clinical phenotype both suggest that Goosecoid is a downstream effector of the regulatory networks that define neural-crest cell-fate specification and subsequent mesoderm cell lineages in mammals, particularly during shoulder and hip formation. The findings confirm that Goosecoid has an essential role in human craniofacial and joint development and suggest that Goosecoid is an essential regulator of mesodermal patterning in mammals and that it has specific functions in neural crest cell derivatives (Parry, 2013).
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