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Home  ›  What Is The Role Of Hox Genes In Animal Development

What Is The Role Of Hox Genes In Animal Development

Written By Sunday, June 12, 2022 Add Comment Edit

Grouping of genes

Hox genes, a subset of homeobox genes, are a group of related genes that specify regions of the body plan of an embryo along the head-tail axis of animals. Hox proteins encode and specify the characteristics of 'position', ensuring that the correct structures form in the correct places of the trunk. For example, Hox genes in insects specify which appendages course on a segment (for case, legs, antennae, and wings in fruit flies), and Hox genes in vertebrates specify the types and shape of vertebrae that will form. In segmented animals, Hox proteins thus confer segmental or positional identity, just practice non form the actual segments themselves.

Studies on Hox genes in ciliated larvae have shown they are only expressed in future adult tissues. In larvae with gradual metamorphosis the Hox genes are activated in tissues of the larval body, more often than not in the body region, that will be maintained through metamorphosis. In larvae with complete metamorphosis the Hox genes are mainly expressed in juvenile rudiments and are absent in the transient larval tissues. The larvae of the hemichordate species Schizocardium californicum and the pilidium larva of Nemertea do not express Hox genes.[one] [ii]

An analogy for the Hox genes can be made to the role of a play director who calls which scene the actors should comport out side by side. If the play director calls the scenes in the wrong society, the overall play will be presented in the wrong order. Similarly, mutations in the Hox genes can result in torso parts and limbs in the wrong place along the trunk. Like a play director, the Hox genes exercise non act in the play or participate in limb formation themselves.

The protein product of each Hox factor is a transcription factor. Each Hox gene contains a well-conserved Dna sequence known as the homeobox, of which the term "Hox" was originally a contraction. Even so, in current usage the term Hox is no longer equivalent to homeobox, because Hox genes are not the only genes to possess a homeobox sequence: humans take over 200 homeobox genes of which 39 are Hox genes.[3] [4] Hox genes are thus a subset of the homeobox transcription factor genes. In many animals, the organization of the Hox genes in the chromosome is the same as the guild of their expression along the anterior-posterior axis of the developing animal, and are thus said to brandish colinearity.[5] [vi] Production of Hox gene products at wrong location in the trunk is associated with metaplasia and predisposes to oncological affliction, e.g. Barrett'south esophagus is the result of altered Hox coding and is a precursor to esophageal cancer.[vii]

Biochemical function [edit]

The products of Hox genes are Hox proteins. Hox proteins are a subset of transcription factors, which are proteins that are capable of binding to specific nucleotide sequences on Deoxyribonucleic acid called enhancers through which they either activate or repress hundreds of other genes. The same Hox poly peptide can act equally a repressor at i gene and an activator at another. The ability of Hox proteins to bind DNA is conferred past a part of the protein referred to as the homeodomain. The homeodomain is a sixty-amino-acid-long DNA-binding domain (encoded past its corresponding 180-base-pair Deoxyribonucleic acid sequence, the homeobox). This amino acrid sequence folds into a "helix-turn-helix" (i.e. homeodomain fold) motif that is stabilized by a third helix. The consensus polypeptide concatenation is shown below:[8] Hox proteins often human action in partnership with co-factors, such as PBC and Meis proteins encoded by very different types of homeobox gene.[nine] 

          Helix i          Helix 2         Helix 3/four          ______________    __________    _________________ RRRKRTAYTRYQLLELEKEFLFNRYLTRRRRIELAHSLNLTERHIKIWFQNRRMKWKKEN ....|....|....|....|....|....|....|....|....|....|....|....|          10        twenty        30        xl        50        lx

Conservation [edit]

Expression of Hox genes in the body segments of different groups of arthropod. The Hox genes vii, 8, and 9 correspond in these groups but are shifted (past heterochrony) by upwards to iii segments. Segments with maxillopeds accept Hox gene 7. Fossil trilobites probably had three body regions, each with a unique combination of Hox genes.

Homeobox genes, and thus the homeodomain protein motif, are found in most eukaryotes. The Hox genes, being a subset of homeobox genes, arose more recently in evolution inside the fauna kingdom or Metazoa. Within the animal kingdom, Hox genes are present across the bilateria[ten] (animals with a clear head-to-tail axis), and take as well been found in Cnidaria such as sea anemones.[11] This implies that Hox genes arose over 550 million years ago. In bilateria, Hox genes are often arranged in factor clusters, although there are many exceptions where the genes have been separated by chromosomal rearrangements.[12] Comparison homeodomain sequences between Hox proteins often reveals greater similarity between species than within a species; this observation led to the conclusion that Hox factor clusters evolved early in animal evolution from a single Hox gene via tandem duplication and subsequent difference, and that a prototypic Hox gene cluster containing at least vii unlike Hox genes was present in the common ancestor of all bilaterian animals.[10] [13]

In near bilaterian animals, Hox genes are expressed in staggered domains along the caput-to-tail centrality of the embryo, suggesting that their role in specifying position is a shared, ancient feature.[fourteen] The functional conservation of Hox proteins tin can be demonstrated by the fact that a wing can function to a big degree with a craven Hox protein in place of its own.[15] Then, despite having a final common antecedent that lived over 550 million years ago,[16] the chicken and fly version of the same Hox factor are like enough to target the aforementioned downstream genes in flies.

In Drosophila [edit]

Homeobox (Hox) gene expression in Drosophila melanogaster

Drosophila melanogaster is an important model for understanding body plan generation and development. The full general principles of Hox gene function and logic elucidated in flies will employ to all bilaterian organisms, including humans. Drosophila, like all insects, has eight Hox genes. These are clustered into ii complexes, both of which are located on chromosome 3. The Antennapedia complex (not to be dislocated with the Antp gene) consists of five genes: labial (lab), proboscipedia (pb), deformed (Dfd), sex combs reduced (Scr), and Antennapedia (Antp). The Bithorax circuitous, named after the Ultrabithorax gene, consists of the remaining iii genes: Ultrabithorax (Ubx), abdominal-A (abd-A) and abdominal-B (abd-B).

Labial [edit]

The lab gene is the almost anteriorly expressed gene. It is expressed in the head, primarily in the intercalary segment (an appendageless segment between the antenna and mandible), and besides in the midgut. Loss of office of lab results in the failure of the Drosophila embryo to internalize the mouth and caput structures that initially develop on the outside of its body (a process called head involution). Failure of caput involution disrupts or deletes the salivary glands and throat. The lab gene was initially and so named considering it disrupted the labial appendage; however, the lab gene is not expressed in the labial segment, and the labial bagginess phenotype is likely a issue of the broad disorganization resulting from the failure of head involution.[17]

Proboscipedia [edit]

The atomic number 82 gene is responsible for the formation of the labial and maxillary palps. Some evidence shows pb interacts with Scr.[18]

Deformed [edit]

The Dfd gene is responsible for the formation of the maxillary and mandibular segments in the larval head.[19] The mutant phenotypes of Dfd are like to those of labial. Loss of function of Dfd in the embryo results in a failure of head involution (see labial gene), with a loss of larval caput structures. Mutations in the developed take either deletions of parts of the head or transformations of head to thoracic identity.[17]

Sex activity combs reduced [edit]

The Scr gene is responsible for cephalic and thoracic development in Drosophila embryo and adult.[twenty]

Antennapedia [edit]

The second thoracic segment, or T2, develops a pair of legs and a pair of wings. The Antp gene specifies this identity by promoting leg formation and allowing (simply not directly activating) fly germination. A ascendant Antp mutation, caused by a chromosomal inversion, causes Antp to be expressed in the antennal imaginal disc, so that, instead of forming an antenna, the disc makes a leg, resulting in a leg coming out of the wing'south head.[ commendation needed ]

Ultrabithorax [edit]

The third thoracic segment, or T3, bears a pair of legs and a pair of halteres (highly reduced wings that function in balancing during flight). Ubx patterns T3 largely by repressing genes involved in wing germination. The wing blade is composed of ii layers of cells that adhere tightly to one some other, and are supplied with nutrient past several wing veins. One of the many genes that Ubx represses is blistered, which activates proteins involved in cell-cell adhesion, and spalt, which patterns the placement of wing veins. In Ubx loss-of-role mutants, Ubx no longer represses wing genes, and the halteres develop as a second pair of wings, resulting in the famous four-winged flies. When Ubx is misexpressed in the second thoracic segment, such every bit occurs in flies with the "Cbx" enhancer mutation, it represses fly genes, and the wings develop every bit halteres, resulting in a iv-haltered fly.[ commendation needed ]

Abdominal-A [edit]

In Drosophila, abd-A is expressed along most of the abdomen, from abdominal segments 1 (A1) to A8. Expression of abd-A is necessary to specify the identity of about of the abdominal segments. A major function of abd-A in insects is to repress limb germination. In abd-A loss-of-function mutants, abdominal segments A2 through A8 are transformed into an identity more like A1. When abd-A is ectopically expressed throughout the embryo, all segments inductive of A4 are transformed to an A4-like abdominal identity.[17] The abd-A gene also affects the blueprint of cuticle generation in the ectoderm, and blueprint of muscle generation in the mesoderm.[18]

Abdominal-B [edit]

Gene abd-B is transcribed in 2 different forms, a regulatory poly peptide, and a morphogenic protein. Regulatory abd-B suppress embryonic ventral epidermal structures in the eighth and 9th segments of the Drosophila abdomen. Both the regulatory protein and the morphogenic poly peptide are involved in the development of the tail segment.[eighteen]

Classification of Hox proteins [edit]

Proteins with a high degree of sequence similarity are too generally assumed to exhibit a loftier caste of functional similarity, i.e. Hox proteins with identical homeodomains are assumed to have identical DNA-binding properties (unless additional sequences are known to influence DNA-bounden). To identify the set of proteins between two unlike species that are most likely to be most similar in function, classification schemes are used. For Hox proteins, three different classification schemes exist: phylogenetic inference based, synteny-based, and sequence similarity-based.[21] The three classification schemes provide conflicting information for Hox proteins expressed in the middle of the body centrality (Hox6-8 and Antp, Ubx and abd-A). A combined approach used phylogenetic inference-based information of the different species and plotted the protein sequence types onto the phylogenetic tree of the species. The approach identified the proteins that all-time represent ancestral forms (Hox7 and Antp) and the proteins that stand for new, derived versions (or were lost in an ancestor and are at present missing in numerous species).[22]

Genes regulated by Hox proteins [edit]

Hox genes act at many levels inside developmental factor hierarchies: at the "executive" level they regulate genes that in turn regulate large networks of other genes (like the cistron pathway that forms an appendage). They also directly regulate what are called realisator genes or effector genes that act at the bottom of such hierarchies to ultimately form the tissues, structures, and organs of each segment. Sectionalisation involves such processes as morphogenesis (differentiation of precursor cells into their final specialized cells), the tight association of groups of cells with similar fates, the sculpting of structures and segment boundaries via programmed cell decease, and the movement of cells from where they are first born to where they will ultimately function, then it is not surprising that the target genes of Hox genes promote prison cell sectionalisation, prison cell adhesion, apoptosis, and jail cell migration.[5]

Examples of target genes
Organism Target factor Normal function of target gene Regulated by
Drosophila distal-less activates factor pathway for limb formation ULTRABITHORAX[23]

(represses distal-less)

distal-less activates cistron pathway for limb germination ABDOMINAL-A[23]

(represses distal-less)

decapentaplegic triggers prison cell shape changes in the gut that are

required for normal visceral morphology

ULTRABITHORAX[24]

(activates decapentaplegic)

reaper Apoptosis: localized cell death creates the segmental

boundary betwixt the maxilla and mandible of the head

DEFORMED[25]

(activates reaper)

decapentaplegic prevents the above prison cell changes in more posterior

positions

Intestinal-B[24]

(represses decapentaplegic)

Mouse EphA7 Cell adhesion: causes tight association of cells in

distal limb that will form digit, carpal and tarsal basic

HOX-A13[5]

(activates EphA7)

Cdkn1a Cell cycle: differentiation of myelomonocyte cells into

monocytes (white claret cells), with cell bike arrest

Hox-A10[26]

(activates Cdkn1a)

Enhancer sequences spring by homeodomains [edit]

The Deoxyribonucleic acid sequence spring by the homeodomain protein contains the nucleotide sequence TAAT, with the 5' terminal T being the nearly important for binding.[27] This sequence is conserved in near all sites recognized by homeodomains, and probably distinguishes such locations equally DNA binding sites. The base pairs following this initial sequence are used to distinguish betwixt homeodomain proteins, all of which have similar recognition sites. For instance, the nucleotide following the TAAT sequence is recognized by the amino acrid at position 9 of the homeodomain protein. In the maternal protein Bicoid, this position is occupied past lysine, which recognizes and binds to the nucleotide guanine. In Antennapedia, this position is occupied by glutamine, which recognizes and binds to adenine. If the lysine in Bicoid is replaced by glutamine, the resulting poly peptide will recognize Antennapedia-binding enhancer sites.[28] [29]

Withal, all homeodomain-containing transcription factors bind essentially the aforementioned Dna sequence. The sequence bound by the homeodomain of a Hox protein is merely six nucleotides long, and such a short sequence would exist plant at random many times throughout the genome, far more than the number of actual functional sites. Specially for Hox proteins, which produce such dramatic changes in morphology when misexpressed, this raises the question of how each transcription cistron tin produce such specific and different outcomes if they all bind the same sequence. One machinery that introduces greater DNA sequence specificity to Hox proteins is to bind protein cofactors. Two such Hox cofactors are Extradenticle (Exd) and Homothorax (Hth). Exd and Hth bind to Hox proteins and appear to induce conformational changes in the Hox protein that increment its specificity.[30]

Regulation of Hox genes [edit]

Just equally Hox genes regulate realisator genes, they are in plow regulated themselves past other genes. In Drosophila and some insects (but not most animals), Hox genes are regulated past gap genes and pair-rule genes, which are in their turn regulated past maternally-supplied mRNA. This results in a transcription factor cascade: maternal factors activate gap or pair-dominion genes; gap and pair-rule genes activate Hox genes; then, finally, Hox genes activate realisator genes that cause the segments in the developing embryo to differentiate.

Regulation is achieved via protein concentration gradients, called morphogenic fields. For example, high concentrations of i maternal protein and low concentrations of others volition turn on a specific set of gap or pair-rule genes. In flies, stripe 2 in the embryo is activated by the maternal proteins Bicoid and Hunchback, simply repressed by the gap proteins Giant and Kruppel. Thus, stripe 2 will but course wherever there is Bicoid and Hunchback, just non where there is Giant and Kruppel.[31]

MicroRNA strands located in Hox clusters accept been shown to inhibit more than inductive hox genes ("posterior prevalence phenomenon"), perchance to ameliorate fine melody its expression blueprint.[32]

Non-coding RNA (ncRNA) has been shown to be abundant in Hox clusters. In humans, 231 ncRNA may exist nowadays. One of these, HOTAIR, silences in trans (it is transcribed from the HOXC cluster and inhibits late HOXD genes) by binding to Polycomb-group proteins (PRC2).[33]

The chromatin construction is essential for transcription but it also requires the cluster to loop out of the chromosome territory.[34]

In higher animals including humans, retinoic acid regulates differential expression of Hox genes along the anteroposterior axis.[35] Genes in the iii' ends of Hox clusters are induced by retinoic acid resulting in expression domains that extend more anteriorly in the body compared to 5' Hox genes that are not induced past retinoic acid resulting in expression domains that remain more posterior.

Quantitative PCR has shown several trends regarding colinearity: the system is in equilibrium and the total number of transcripts depends on the number of genes nowadays according to a linear relationship.[36]

Collinearity [edit]

In some organisms, specially vertebrates, the diverse Hox genes are situated very close to one another on the chromosome in groups or clusters. The order of the genes on the chromosome is the same every bit the expression of the genes in the developing embryo, with the beginning gene beingness expressed in the anterior end of the developing organism. The reason for this colinearity is not nevertheless completely understood, but could be related to the activation of Hox genes in a temporal sequence past gradual unpacking of chromatin along a gene cluster. The diagram in a higher place shows the relationship between the genes and poly peptide expression in flies.[ commendation needed ]

Nomenclature [edit]

The Hox genes are named for the homeotic phenotypes that result when their function is disrupted, wherein one segment develops with the identity of another (e.g. legs where antennae should be). Hox genes in different phyla take been given different names, which has led to confusion almost nomenclature. The complement of Hox genes in Drosophila is fabricated up of 2 clusters, the Antennapedia complex and the Bithorax circuitous, which together were historically referred to as the HOM-C (for Homeotic Complex). Although historically HOM-C genes have referred to Drosophila homologues, while Hox genes referred to vertebrate homologues, this distinction is no longer made, and both HOM-C and Hox genes are chosen Hox genes.[ citation needed ]

In other species [edit]

Hox genes in various species

Vertebrates [edit]

Mice and humans have 39 Hox genes in iv clusters:[37] [38]

Cluster Man Chromosome Genes
HOXA@ chromosome 7 HOXA1, HOXA2, HOXA3, HOXA4, HOXA5, HOXA6, HOXA7, HOXA9, HOXA10, HOXA11, HOXA13
HOXB@ chromosome 17 HOXB1, HOXB2, HOXB3, HOXB4, HOXB5, HOXB6, HOXB7, HOXB8, HOXB9, HOXB13
HOXC@ chromosome 12 HOXC4, HOXC5, HOXC6, HOXC8, HOXC9, HOXC10, HOXC11, HOXC12, HOXC13
HOXD@ chromosome ii HOXD1, HOXD3, HOXD4, HOXD8, HOXD9, HOXD10, HOXD11, HOXD12, HOXD13

The ancestors of vertebrates had a single Hox cistron cluster,[39] [40] [ commendation needed ] which was duplicated (twice) early in vertebrate evolution by whole genome duplications to requite four Hox factor clusters: Hoxa, Hoxb, Hoxc and Hoxd. It is currently unclear whether these duplications occurred before or after divergence of lampreys and hagfish from the rest of vertebrates.[41] Near mammals, amphibians, reptiles and birds take four HOX clusters, while near teleost fish, including zebrafish and medaka, have seven or eight Hox gene clusters because of an additional genome duplication which occurred in their evolutionary history.[42] [37] In zebrafish, ane of the 8 Hox factor clusters (a Hoxd cluster) has lost all protein-coding genes, and just a single microRNA gene marks the location of the original cluster.[43] In some teleost fish, such every bit salmon, an even more recent genome duplication occurred, doubling the seven or 8 Hox gene clusters to requite at least 13 clusters [44]

Vertebrate bodies are non segmented in the aforementioned way as insects; they are on average much more complex, leading to more infrastructure in their body plan compared to insects.   HOX genes control the regulation and development of a lot of primal structure is the body such every bit: somites, which form vertebrae and ribs, the dermis of the dorsal peel, the skeletal muscles of the back, and the skeletal muscles of the body wall and limbs.  HOX genes help differentiate somite cells into more specific identities and straight them to develop differently depending on where they are in the body.[45] A large deviation betwixt vertebrates and invertebrates is the location and layering of HOX genes. The key mechanisms of development are strongly conserved among vertebrates from fish to mammals.

Due to the fact that the HOX genes is and so highly conserved, well-nigh research has been done on much simpler model organisms, such equally mice.  1 of the major differences that was noticed when comparison mice and drosophila, in particular, has to do with the location and layering of HOX genes within the genome. Vertebrates practice have HOX genes that are homologous to those of the fly as information technology is 1 of the most highly conserved genes, but the location is different. For case, there are more HOX genes on the v' side of the mouse segment compared to the invertebrates.[46]  These genes represent to expression in the tail, which would make sense as flies would not take anything similar to the tail that all vertebrates have. Additionally, in well-nigh vertebrates there are 39 members segregated into four separate tightly clustered gene arrays (A–D) on iv separate chromosomes, whereas in that location are eight HOX genes in total for the Drosophila.[47] Clusters are far more redundant and less likely to generate mutations. In flies, i gene tin can exist mutated, resulting in a haltere, something central for them to exist able to fly, beingness transformed into a fly, or an antenna turning into a leg; in the mouse, two to 4 genes must be simultaneously removed to go a similar complete transformation.  Some researchers believe that, considering of the back-up of the vertebrate HOX cluster plan and more constrained compared to invertebrate HOX clusters, the evolvability of vertebrate HOX clusters is, for some structural or functional reason,  far lower than their invertebrate counterparts.[48] This rapid evolvability is in function because  invertebrates experienced much more dramatic episodes of adaptive radiation and mutations. More than than 20 major clades of invertebrates differ so radically in torso organisation, partly due to a college mutation rate, that they became formally classified every bit different phyla.[49]  All of the paralogous genes need to be knocked out in club for there to be any phenotypic changes for the most role. This is also 1 reason why homeotic mutations in vertebrates are so rarely seen.

In mouse embryos, the HOX10 genes, which is one of the genes that lie in the tail portion of the animate being, turn the "rib-edifice" system off when the cistron is activated. The genes are active in the lower back, where the vertebrae don't abound ribs, and inactive in the mid-back, allowing ribs to be formed.  When the HOX10 paralogs are experimentally inactivated, the vertebrae of the lower dorsum grow ribs.[50] This research prompted an evolutionary search for these mutations among all animals.  An instance of this is in lizards and snakes. In snakes, HOX10 genes have lost their rib-blocking ability in that way.[51]

Amphioxus [edit]

Amphioxus such as Branchiostoma floridae accept a single Hox cluster with 15 genes, known as AmphiHox1 to AmphiHox15.[52]

Other invertebrates [edit]

Vi Hox genes are dispersed in the genome of Caenorhabditis elegans, a roundworm.[10] : fig. iii Hydra and Nematostella vectensis, both in the Phylum Cnidaria, have a few Hox/ParaHox-like homeobox genes.[53] [11]

Hox gene expression has as well been studied in brachiopods,[54] annelids, [55] and a suite of molluscs.[56]

History [edit]

The Hox genes are so named because mutations in them crusade homeotic transformations. Homeotic transformations were first identified and studied by William Bateson in 1894, who coined the term "homeosis". After the rediscovery of Mendel'southward genetic principles, Bateson and others realized that some examples of homeosis in floral organs and animal skeletons could be attributed to variation in genes.

Definitive evidence for a genetic basis of some homeotic transformations was obtained by isolating homeotic mutants. The beginning homeotic mutant was found by Calvin Bridges in Thomas Hunt Morgan's laboratory in 1915. This mutant shows a partial duplication of the thorax and was therefore named Bithorax (bx). It transforms the third thoracic segment (T3) toward the second (T2). Bithorax arose spontaneously in the laboratory and has been maintained continuously as a laboratory stock ever since.[57]

The genetic studies by Morgan and others provided the foundation for the systematic analyses of Edward B. Lewis and Thomas Kaufman, which provided preliminary definitions of the many homeotic genes of the Bithorax and Antennapedia complexes, and likewise showed that the mutant phenotypes for most of these genes could be traced back to patterning defects in the embryonic body plan.

Ed Lewis, Christiane Nüsslein-Volhard and Eric F. Wieschaus identified and classified 15 genes of key importance in determining the body programme and the formation of body segments of the fruit wing D. melanogaster in 1980.[58] For their work, Lewis, Nüsslein-Volhard, and Wieschaus were awarded the Nobel Prize in Physiology or Medicine in 1995.[59]

In 1983, the homeobox was discovered independently by researchers in 2 labs: Ernst Hafen, Michael Levine, and William McGinnis (in Walter Gehring's lab at the University of Basel, Switzerland) and Matthew P. Scott and Amy Weiner (in Thomas Kaufman's lab at Indiana Academy in Bloomington).

Future [edit]

Hox genes play disquisitional roles in the development of structures such as limbs, lungs, the nervous arrangement, and eyes. As T. R. Lappin and colleagues observed in 2006, "Evolutionary conservation provides unlimited telescopic for experimental investigation of the functional control of the Hox gene network which is providing important insights into human illness." In the hereafter, more inquiry can be washed in investigating the roles of Hox genes in Leukaemia and cancer (such as EOC).[37]

See also [edit]

  • Homeotic factor
  • Hox genes in amphibians and reptiles
  • Morphogenesis
  • Discredited hypotheses for the Cambrian explosion (Section: Regulatory genes)

References [edit]

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Further reading [edit]

  • Chase P (1998). "The Function of Hox Genes". In Bittar EE (ed.). Developmental Biology. Elsevier. ISBN978-1-55938-816-0.

Source: https://en.wikipedia.org/wiki/Hox_gene#:~:text=Hox%20genes%2C%20a%20subset%20of,correct%20places%20of%20the%20body.

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