How does the colinearity of the HOX genes determine the body plan of an organism?

How does the colinearity of the HOX genes determine the body plan of an organism?

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I was recently reading about colinearity in the HOX genes that give an organism its high-level body plan (where the order of the HOX genes on the chromosome follow the head-to-tail order of body segments, such that the head gene comes before the thorax gene, comes before the abdomen gene, etc).

I'm really just a layman interested in this stuff (only completed A & P I), but I was under the impression that the location of genes on a chromosome has no bearing on the expression of those genes or phenotype of the organism -- in other words, that genes can be anywhere on any chromosome.

Do we understand how the order of the HOX genes ends up being expressed as the order of the body segments? Do we know why the positioning of these genes matters when the order of other genes don't?

You might be interested in this book

When writing Hox Gene collinearity (or colinearity as it is often misspelled as explain in wiki!) on Google scholar or WebOfKnowledge you will get many results on the subject. It is still today an ongoing debate.

Below are some sentences I pick up from these articles. It is certainly hard to understand as I hardly understood what I wrote! The best for you is to go through this review. It is not easy (at least for me but it is not at all my field) but I think it is the best source of information you can find on the subject.

This and this might also help you to understand the debate on the subject.

There are several types of collinearity:

Spatial collinearityis the sequential 3' to 5' expression of Hox Genes along a body axis.Spatial collinearitycan be associated with time dependence where the most 3' is expressed first. This is defined astemporal collinearity.

There are two main models to explain the mechanisms hidden behind this ordering.

  • 1) Collinearity is based on transcriptional regulation and specifically that is limited by the progressive 3' to 5' opening of Hox cluster chromatin and/or mediated by global control regions

  • 2) Collinearity depends on interactions between the Hox genes themselves. These interactions include 'posterior prevalence', a negative interaction among Hox proteins that clearly relates to functional collinearity in Drosophila.


It is suggested that collinearity evolved by repeated tandem duplication of an ancestral ur-Hox Gene

Quoting from some parts of Sean Carroll's book - Endless forms most beautiful, I have tried to provide you with an answer but, remember that this can never suffice for the reading of this great book.

Yes, we do understand how the hox genes' expression is regulated.

From page 126-127

… The establishment of these Hox zones and their subsequent action in sculpting the different forms of repeated parts is the fundamental genetic logic upon which the modular forms of large,biletarian animals is built.

The genetic logic relies on genetic switches at two levels. One set of switches belongs to the Hox genes themselves. these switches activate each Hox gene in different zones that will become different modules of the animal. Another set of switches contain signature sequences that are recognized by Hox proteins and that control how other genes are expressed in different modules.

In both arthropods and vertebrates, the Hox genes are developed in zones along the main body axis. The distinct zones of each Hox gene's expression domain are governed by genetic switches, and seperate switches control Hox gene patterns in different tissues such as the… Because of the logic of the genetic switches, the cells that belong to one module express different Hox proteins or combinations of Hox proteins than those in adjacent modules…

Let us take an example of Ubx gene which leads to formation of wings in the 2nd and 3rd thoracic segments of drosophila. This gene is turned off in the first thoracic segment but in the second and third segments, it is turned on. This regulation can be achieved because of the genetic switches which in turn can be switched on or off by activators and repressors. These activators and repressors are unevenly distributed in the embryo and so regulation of switches in different parts of the embryo is possible.

I have suggested that collinearity of Hox genes is a mechanism to maximise physical segregation between active and inactive Hox genes within the Hox gene cluster. This is to minimise interference between Hox genes in these two states. See 'The significance of Hox gene collinearity' in Int. J. Dev. Biol. 2015 Vol 59, pp 159-170. Or download from

How does the colinearity of the HOX genes determine the body plan of an organism? - Biology

Since the early nineteenth century, scientists have observed that many animals, from the very simple to the complex, shared similar embryonic morphology and development. Surprisingly, a human embryo and a frog embryo, at a certain stage of embryonic development, look remarkably alike! For a long time, scientists did not understand why so many animal species looked similar during embryonic development but were very different as adults. They wondered what dictated the developmental direction that a fly, mouse, frog, or human embryo would take. Near the end of the twentieth century, a particular class of genes was discovered that had this very job. These genes that determine animal structure are called “homeotic genes,” and they contain DNA sequences called homeoboxes. Genes with homeoboxes encode protein transcription factors. One group of animal genes containing homeobox sequences is specifically referred to as Hox genes . This cluster of genes is responsible for determining the general body plan, such as the number of body segments of an animal, the number and placement of appendages, and animal head-tail directionality. The first Hox genes to be sequenced were those from the fruit fly (Drosophila melanogaster). A single Hox mutation in the fruit fly can result in an extra pair of wings or even legs growing from the head in place of antennae (this is because antennae and legs are embryologic homologous structures and their appearance as antennae or legs is dictated by their origination within specific body segments of the head and thorax during development). Now, Hox genes are known from virtually all other animals as well.

Figure 1. Shown here is the homology between Hox genes in mice and humans. Note how Hox gene expression, as indicated with orange, pink, blue, and green shading, occurs in the same body segments in both the mouse and the human. While at least one copy of each Hox gene is present in humans and other vertebrates, some Hox genes are missing in some chromosomal sets.

While there are a great many genes that play roles in the morphological development of an animal, including other homeobox-containing genes, what makes Hox genes so powerful is that they serve as “master control genes” that can turn on or off large numbers of other genes. Hox genes do this by encoding transcription factors that control the expression of numerous other genes. Hox genes are homologous across the animal kingdom, that is, the genetic sequences of Hox genes and their positions on chromosomes are remarkably similar across most animals because of their presence in a common ancestor, from worms to flies, mice, and humans (Figure 1).

Hox genes are highly conserved genes encoding transcription factors that determine the course of embryonic development in animals. In vertebrates, the genes have been duplicated into four clusters: Hox-A, Hox-B, Hox-C, and Hox-D. Genes within these clusters are expressed in certain body segments at certain stages of development.

In addition, the order of the genes reflects the anterior-posterior axis of the animal’s body. One of the contributions to increased animal body complexity is that Hox genes have undergone at least two and perhaps as many as four duplication events during animal evolution, with the additional genes allowing for more complex body types to evolve. All vertebrates have four (or more) sets of Hox genes, while invertebrates have only one set.

Practice Question

If a Hox 13 gene in a mouse was replaced with a Hox 1 gene, how might this alter animal development?

Two of the five clades within the animal kingdom do not have Hox genes: the Ctenophora and the Porifera. In spite of the superficial similarities between the Cnidaria and the Ctenophora, the Cnidaria have a number of Hox genes, but the Ctenophora have none. The absence of Hox genes from the ctenophores has led to the suggestion that they might be “basal” animals, in spite of their tissue differentiation. Ironically, the Placozoa, which have only a few cell types, do have at least one Hox gene. The presence of a Hox gene in the Placozoa, in addition to similarities in the genomic organization of the Placozoa, Cnidaria and Bilateria, has led to the inclusion of the three groups in a “Parahoxozoa” clade. However, we should note that at this time the reclassification of the Animal Kingdom is still tentative and requires much more study.

Animal Body Planes and Cavities

Animal body plans follow set patterns related to symmetry. They are asymmetrical, radial, or bilateral in form as illustrated in Figure 6. Asymmetrical animals are animals with no pattern or symmetry an example of an asymmetrical animal is a sponge. Radial symmetry, as illustrated in Figure 6, describes when an animal has an up-and-down orientation: any plane cut along its longitudinal axis through the organism produces equal halves, but not a definite right or left side. This plan is found mostly in aquatic animals, especially organisms that attach themselves to a base, like a rock or a boat, and extract their food from the surrounding water as it flows around the organism. Bilateral symmetry is illustrated in the same figure by a goat. The goat also has an upper and lower component to it, but a plane cut from front to back separates the animal into definite right and left sides. Additional terms used when describing positions in the body are anterior (front), posterior (rear), dorsal (toward the back), and ventral (toward the stomach). Bilateral symmetry is found in both land-based and aquatic animals it enables a high level of mobility.

Figure 6. Animals exhibit different types of body symmetry. The sponge is asymmetrical, the sea anemone has radial symmetry, and the goat has bilateral symmetry.

A standing vertebrate animal can be divided by several planes. A sagittal plane divides the body into right and left portions. A midsagittal plane divides the body exactly in the middle, making two equal right and left halves. A frontal plane (also called a coronal plane) separates the front from the back. A transverse plane (or, horizontal plane) divides the animal into upper and lower portions. This is sometimes called a cross section, and, if the transverse cut is at an angle, it is called an oblique plane. Figure 7 illustrates these planes on a goat (a four-legged animal) and a human being.

Figure 7. Shown are the planes of a quadruped goat and a bipedal human. The midsagittal plane divides the body exactly in half, into right and left portions. The frontal plane divides the front and back, and the transverse plane divides the body into upper and lower portions.

Vertebrate animals have a number of defined body cavities, as illustrated in Figure 8. Two of these are major cavities that contain smaller cavities within them. The dorsal cavity contains the cranial and the vertebral (or spinal) cavities. The ventral cavity contains the thoracic cavity, which in turn contains the pleural cavity around the lungs and the pericardial cavity, which surrounds the heart. The ventral cavity also contains the abdominopelvic cavity, which can be separated into the abdominal and the pelvic cavities.

Figure 8. Vertebrate animals have two major body cavities. The dorsal cavity contains the cranial and the spinal cavity. The ventral cavity contains the thoracic cavity and the abdominopelvic cavity. The thoracic cavity is separated from the abdominopelvic cavity by the diaphragm. The abdominopelvic cavity is separated into the abdominal cavity and the pelvic cavity by an imaginary line parallel to the pelvis bones. (credit: modification of work by NCI)

Theories, Development, Invertebrates

F. Hirth , H. Reichert , in Evolution of Nervous Systems , 2007 A Tripartite Organization of the Insect and Chordate Brain?

The conserved expression and function of otd/Otx and Hox genes suggest that invertebrate and vertebrate brains are all characterized by a rostral region specified by genes of the otd/Otx family and a caudal region specified by genes of the Hox family. However, in ascidians and vertebrates, a Pax2/5/8 expression domain is located between the anterior Otx and the posterior Hox expression regions of the embryonic brain ( Holland and Holland, 1999 Wada and Satoh, 2001 ). In vertebrate brain development, this Pax2/5/8 expression domain is an early marker for the isthmic organizer positioned at the midbrain–hindbrain boundary (MHB), which controls the development of the midbrain and the anterior hindbrain ( Liu and Joyner, 2001 Rhinn and Brand, 2001 Wurst and Bally-Cuif, 2001 ). The central role of this MHB region in brain development together with the conserved expression patterns of Pax2/5/8 genes in this region have led to the proposal that a fundamental characteristic of the ancestral chordate brain was its tripartite organization characterized by Otx, Pax2/5/8, and Hox gene expressing regions ( Wada et al., 1998 ).

An analysis of brain development in Drosophila has uncovered similarities in the expression and function of the orthologous genes that pattern the vertebrate MHB region ( Hirth et al., 2003 ). Thus, a Pax2/5/8 expressing domain was found to be located between the anterior otd/Otx expressing region and the posterior Hox expressing region in the embryonic brain. In Drosophila, as in vertebrates, this Pax2/5/8 expressing domain is positioned at the interface between the otd/Otx2 expression domain and a posteriorly abutting unplugged/Gbx2 expression domain. Moreover, inactivation of otd/Otx or of unplugged/Gbx2 results in comparable effects on mispositioning or loss of brain-specific expression domains of orthologous genes in both embryonic brain types. These developmental genetic similarities indicate that the tripartite ground plan, which characterizes the developing vertebrate brain, is also at the basis of the developing insect brain ( Figure 6 ). This, in turn, has led to the suggestion that a corresponding, evolutionarily conserved, tripartite organization also characterized the brain of the last common ancestor of insects and chordates ( Hirth et al., 2003 ).

Figure 6 . Tripartite organization of the (a) Drosophila, (b) mouse, and (c) ascidian brain, based on expression patterns of orthologous genes. The expression of otd/Otx2, unpg/Gbx2, Pax2/5/8, and Hox1 gene orthologues in the developing CNS of (a) stage 13/14 Drosophila embryo, (b) stage E10 mouse embryo, and (c) neurula ascidian embryo. In all cases, a Pax2/5/8-expressing domain is located between an anterior otd/Otx2 expressing region and a posterior Hox expressing region in the embryonic brain. Moreover, in Drosophila, as in mouse, a Pax2/5/8-expressing domain is positioned at the interface between the otd/Otx2 expression domain and a posteriorly abutting unplugged/Gbx2 expression domain. This otd/Otx2unpg/Gbx2 interface displays similar developmental genetic features in both Drosophila and mouse. Reproduced from Hirth, F., Kammermeier, L., Frei, E., Walldorf, U., Noll, M., and Reichert, H. 2003. An urbilaterian origin of the tripartite brain: Developmental genetic insights from Drosophila. Development 130, 2365–2373, with permission from The Company of Biologists Ltd.

HOX genes

Homeobox genes are crucial for very early embryonic development and are involved in cell differentiation and general body pattern.


Homeobox genes are crucial for very early embryonic development and are involved in cell differentiation and general body pattern. They are similar in eukaryotic organisms because every organism needs these essential functions, such as developing body structure.

The image below shows HOX genes (homeotic genes) and how they regulate the body structure of both a fly and a human.

All eukaryotes evolved from a common ancestor with these genes and, while they have not remained identical and have evolved over time, their essential functions have remained relevant thus they have been retained.

You can learn more about homeotic genes in general here and you can read about homeotic genes and body structure here.

How does the colinearity of the HOX genes determine the body plan of an organism? - Biology

Section 1: DNA: The Genetic Material

Section 2: Replication of DNA

Section 3: DNA, RNA, and Protein

Section 4: Gene Regulation and Mutation

Click on a lesson name to select.

  • Concluded that the viral DNA was injected into the cell and provided the genetic information needed to produce new viruses

deoxyribose and phosphate

other by three hydrogen bonds

other by two hydrogen bonds

  • The chromatin fibers supercoil to form chromosomes that are visible in the metaphase stage of mitosis.
  • Parental strands of DNA separate, serve as templates, and produce DNA molecules that have one strand of parental DNA and
  • DNA polymerase continues adding appropriate nucleotides to the chain by adding to the 3′ end of the new DNA strand.
  • The lagging strand is synthesized discontinuously into small segments, called Okazaki fragments .

Comparing DNA Replication in Eukaryotes and Prokaryotes

polymerase binds to a specific section where an

  • The Beadle and Tatum experiment showed that one gene codes for one enzyme. We now know that one gene codes for one polypeptide.

Gene Regulation and Mutation

Prokaryote Gene Regulation

  • An operon is a section of DNA that contains the genes for the proteins needed for a specific metabolic pathway.

Gene Regulation and Mutation

Gene Regulation and Mutation

Eukaryote Gene Regulation

  • Transcription factors ensure that a gene is used at the right time and that proteins are made in the right amounts

Gene Regulation and Mutation

Gene Regulation and Mutation

Gene Regulation and Mutation

Gene Regulation and Mutation

Gene Regulation and Mutation

Protein Folding and Stability

Gene Regulation and Mutation

Gene Regulation and Mutation

Body-cell v. Sex-cell Mutation

  • Mutations that occur in sex cells are passed on to the organism’s offspring and will be present in every cell of the offspring.

Gene Regulation and Mutation

Click on a hyperlink to view the corresponding feature.

Which scientist(s) definitively proved

that DNA transfers genetic material?

Chapter Diagnostic Questions

Chapter Diagnostic Questions

Name the small segments of the lagging

Chapter Diagnostic Questions

  • It contains the sugar ribose.
  • It contains the base uracil.
  • It is single-stranded.
  • It contains a phosphate.

The experiments of Avery, Hershey and

Chase provided evidence that the carrier

of genetic information is _______.

Section 1 Formative Questions

What is the base-pairing rule for purines

and pyrimidines in the DNA molecule?

Section 1 Formative Questions

Section 1 Formative Questions

  • chromatin and histones
  • DNA and protein
  • DNA and lipids
  • protein and centromeres

What are chromosomes composed of?

The work of Watson and Crick solved the mystery of how DNA works as a

Section 2 Formative Questions

Section 2 Formative Questions

Which is not an enzyme involved in DNA

Which shows the basic chain of events

in all organisms for reading and expressing

  • DNA → RNA → protein
  • RNA → DNA → protein
  • mRNA → rRNA → tRNA
  • RNA processing → transcription → translation

Section 3 Formative Questions

Section 3 Formative Questions

In the RNA molecule, uracil replaces

Section 3 Formative Questions

Which diagram shows messenger

Section 3 Formative Questions

What characteristic of the mRNA molecule do scientists not yet understand?

  • intervening sequences in the mRNA molecule called introns
  • the original mRNA made in the nucleus called the pre-mRNA
  • how the sequence of bases in the mRNA molecule codes for amino acids
  • the function of many adenine nucleotides at the 5′ end called the poly-A tail

Why do eukaryotic cells need a complex control system to regulate the expression of genes?

  • All of an organism’s cells transcribe the same genes.
  • Expression of incorrect genes can lead to mutations.
  • Certain genes are expressed more frequently than others are.
  • Different genes are expressed at different times in an
    organism’s lifetime.

Section 4 Formative Questions

Section 4 Formative Questions

Which type of gene causes cells to

become specialized in structure in

Section 4 Formative Questions

What is an immediate result of a mutation

Section 4 Formative Questions

Which is the most highly mutagenic?

Look at the following figure. Identify the proteins that DNA first coils around.

Chapter Assessment Questions

Chapter Assessment Questions

  • They determine size.
  • They determine body plan.
  • They determine sex.
  • They determine number of body segments.

Explain how Hox genes affect an organism.

Explain the difference between body-cell and
sex-cell mutation.

Chapter Assessment Questions

Answer: A mutagen in a body cell becomes

part of the of the genetic sequence

in that cell and in future daughter

cells. The cell may die or simply not

perform its normal function. These

mutations are not passed on to the

next generation. When mutations

occur in sex cells, they will be

present in every cell of the offspring.

What does this diagram show about the replication of DNA in eukaryotic cells?

HOX genes in leukaemia

In many forms of cancer, chromosomal translocations lead to the creation of fusion genes and enforced expression of proto-oncogenes. The fusion products often involve transcriptional regulators which can act as master regulators of cell fate. In leukaemia, elevated levels of HOX genes have been frequently observed, particularly in AML 73-75 . Changes in HOX gene expression are associated with chromosomal translocations involving upstream regulators such as the mixed lineage leukaemia (MLL) gene or, more directly, the fusion of a HOX gene to another such as the nucleoporin gene NUP98. Recent investigations of HOX gene expression in leukaemia have provided important insights into disease classification and prediction of clinical outcome.

MLL in leukaemia

The MLL gene on chromosome 11q23 is the human homologue of Drosophila trithorax (trx), a master regulator of HOX genes essential for patterning during embryogenesis. MLL is a histone methyltransferase which undergoes heterologous fusion with over 40 partner proteins 76 in a variety of haematological malignancies including acute myeloid leukaemia (AML), acute lymphoid leukaemias (ALL) of both B-precursor (B-ALL) and T-lineage (T-ALL) sub-types, and myelodysplastic syndrome (MDS). Specific MLL fusion proteins are often associated with neoplasia affecting cells of a particular lineage. Thus, it appears that the fusion partner is involved in determining disease phenotype.

Chromosomal translocations involving MLL give rise to in-frame gene fusions in which the amino-terminal portion of the encoded MLL protein is fused to the carboxy-terminal portions of the fusion partner. They are present in approximately 10% of acute leukaemias. MLL translocations generally signify a poor prognosis and are frequently found in paediatric leukaemia and in patients who develop secondary leukaemia following treatment with topoisomerase II inhibitors. MLL chimeras may lead to inappropriate maintenance of target gene expression due to recruitment of co-activators of the basal transcriptional machinery 77 .

Numerous studies have been undertaken to examine the downstream consequences of MLL translocations in order to identify selectively expressed genes which might ultimately serve as chemotherapeutic targets. Recently, gene expression patterns in MLL-rearranged T-ALLs and B-ALLs have been investigated. Armstrong et al 78 found characteristic, distinct profiles for patients with B-ALL (which they designated MLL B-ALL) and this was confirmed independently in a large group of patients 79 . Subsequently Ferrando et al 80 examined a group of patients with MLL T-ALL and found that they consistently demonstrated increased expression of a subset of HOX genes, namely HOXA9, HOXA10, and HOXC6, as well as MEIS1, a co-regulator of HOX. This pattern of expression was reiterated in a group of patients with MLL B-ALL. These investigations exemplify many gene expression profiling studies which implicate HOX genes as dominant factors in MLL-rearranged leukaemic transformations.

The regulatory role of MLL in HOX gene expression is supported by phenotypic analyses of mice and flies. In mice haplo-insufficient for Mll, homeotic transformations of the axial skeleton are associated with abnormalities in the maintenance of Hoxa7 and Hoxc9 expression 81 . In Drosophila, the counterpart of MLL, Trx, is required for maintenance of expression of the HOM-C group of genes during embryogenesis. Further proof that MLL is directly involved in the regulation of HOX gene expression comes from the recent demonstration that MLL binds directly to HOX promoter sequences 82 .

HOX fusion genes in leukaemia

NUP98 is a member of the nuclear pore complex and acts as a transporter of proteins and RNA protein complexes between the nucleus and cytoplasm. The propensity of NUP98 to form fusion genes, particularly with members of the HOX gene family, is being increasingly recognized. To date, HOX partners for NUP98 are all Abd-B genes and include HOXA9 83 , 84 , HOXA11 85 , HOXA13 85 , HOXC11 86 , HOXC13 87 , and HOXD13 88 . NUP98–HOX fusions consist of the amino-terminus of NUP98 containing a region of phenylalanine–glycine repeats and the carboxy-terminus of the HOX protein, containing the intact homeodomain. Pineault et al investigated the leukaemogenic potential of NUP98–HOX fusion proteins by engineering fusions with HOX genes not previously identified as fusion partners, and concluded that many, if not all, HOX genes are potentially leukaemogenic 89 .

HOX gene expression in leukaemia

Engineered overexpression of several HOX genes induces leukaemia in animal models and modulated HOX gene expression has been found in patients with leukaemia. In an attempt to reach a molecular classification of leukaemia, using DNA microarray, HOXA9 was identified as a predictive marker for the diagnosis of AML 73 . HOXA9 expression was the only single gene among 6817 tested that showed a strong correlation with clinical outcome its expression was also correlated with treatment failure in patients with AML.

A survey of HOXA9 and MEIS1 gene expression in 24 leukaemic cell lines and 80 patient samples by RNase protection analysis and immunohistochemistry revealed that these genes are commonly co-expressed in myeloid cell lines and in samples from patients with AML, of all types except promyelocytic leukaemia 75 . Multiple HOX genes were overexpressed in AML patients with a poor prognosis compared with those with favourable cytogenetics 90 .

Acute promyelocytic leukaemia (APL) is associated with a reciprocal and balanced translocation involving the formation of a co-repressor complex between the retinoic acid receptor-α (RARα) and a partner such as PML. All-trans retinoic acid (ATRA) is used to treat APL and is a potent morphogen regulating HOX gene expression in embryogenesis. By real-time quantitative PCR (Q-PCR), Thompson et al 91 reported a global down-regulation of 26 HOX genes in patients with APL, and in common with studies on AML 92 , 93 , found that low HOX gene expression is associated with a favourable outcome.

In murine models of leukaemia caused by co-overexpression of a Hox gene with its collaborating TALE family member cofactor (eg Meis1, Pbx1), it has been shown that specific complexes are required to initiate and maintain the leukaemia and that in the collaboration, the TALE family member acts as an accelerator of the leukaemic process and that in the particular collaboration, the HOX gene defines the identity of the leukemia 94 .

Loss of altruism (and a body plan) without a loss of genes

An international team of researchers found that the evolutionary loss of the "altruistic" worker caste in ants is not accompanied by a loss of genes.

Social insects, such as ants, are typically characterized by two distinct female castes: workers and queens. Previous research has found that workers and queens each express different sets of genes leading scientists to speculate that there are worker specific or "altruistic" genes that promote sociality.

Testing this "novel gene" hypothesis is difficult given that all ants are social. However, not all ants make workers. Some ants are "workerless social parasites" whose queens exploit the worker force of other species by invading and setting up shop in their colonies. The authors took advantage of the unusual biology of these ants that have lost their worker caste to determine if worker genes really exist.

The research team, led by Chris R. Smith (Earlham College) and Alexander (Sasha) Mikheyev (Okinawa Institute of Science and Technology), sequenced and compared the genomes of six ants (3 hosts and 3 workerless social parasites) and looked for evidence that genes that are typically over expressed in the worker caste would degenerate through time when workers are no longer produced. Instead of finding degeneration in "worker" genes, they found that there are no "worker" genes and the majority of the protein coding genome is maintained in species that stopped producing workers even after one million years. Their research is online early in the journal Molecular Biology and Evolution.

"This was a total surprise, we hypothesized the opposite -- when you lose a trait then the genes for that trait should disappear over time," said Smith. "This result has two interesting implications: first, there don't seem to be any genes that are explicitly 'worker' and thus truly 'altruistic', and two, that the loss of an entire body plan is not accompanied by a loss of genes."

This result suggests that any organism's genome may harbor the potential to produce historic phenotypes that are no longer under selection (for

1 million years) -- one need only speculate about what ancient human traits may continue to lurk in our own genomes, waiting to be expressed in a different environmental context.

When looking across developmental stages in an ant (the red harvester ant, Pogonomyrmex barbatus), the researchers found that most genes are expressed in both queens and workers, but often at different points in development. For example, there are no uniquely "worker" or "queen" genes. They then looked at whether genes with a greater bias in workers were more likely to get lost in species that no longer produce workers (social parasites).

To do this the researchers sequenced the genomes of two host species and two of their social parasites. The answer was no, the entire protein coding genome was under selection to maintain the genes present in both hosts and workerless social parasites.

The researchers found their results so surprising that they sequenced the genomes of another host-social parasite pair in the genus Vollenhovia, which are evolutionarily independent. Once again, the result was the same. Again surprised, they tested whether they could even expect to see the deterioration of genes in the mere 700,000 to million years of divergence between worker and worker-less species. Indeed, models do predict gene loss, yet none was evident in their actual samples.

"Social parasitism is relatively widespread in social insects, and our results suggest why -- most changes are regulatory, and don't require complex genome-wide alterations," Mikheyev said.

The results reported in this new research add to a growing body of literature suggesting that many traits (and whole body plans) may evolve by tweaks in the regulation of pre-existing genes and networks. Phenotype gain and loss may be facilitated by changes in the environment within and outside of the organism, not necessarily requiring changes to protein coding genes, just changes to when and how they are used).

"This research reminds us of the importance of studying organisms with unusual natural history in order to get insight into the processes that govern diversity more generally," said Andrew Suarez from the University of Illinois and a co-author of the study.

While this work was on species far removed from the origin of sociality, it does suggest that sociality may have evolved from regulatory changes in a solitary ancestor rather than requiring novel altruism genes for social living and division of labor.


The authors thank Prof. Ettore Olmo and the anonymous reviewers for their helpful comments on the manuscript.

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Watch the video: Nipam Patel MBL 1: Patterning the Anterior-Posterior Axis: The Role of Homeotic Hox Genes (February 2023).