Nested Gene
Related terms:
Cladistics
Phenotype
Gene Expression
Proteins
Exons
Introns
DNA
RNA
Alternative Splicing
Factor VIII
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Selective Breeding
Nihar Ranjan Chattopadhyay, in Induced Fish Breeding, 2017
4.8 Effect of Stock Transfer on Fish Biodiversity
Protein electrophoresis and nested gene diversity analysis (Gyllensten, 1985) suggest that the possibility for adverse genetic consequences of stock transfers is greater for freshwater fish (29.4%) compare to marine fish (1.6%). Experience with two subspecies of large-mouth bass and their hybrids, when they are raised in the native environment of northern species, showed that there is maximum probability for the introduced species to contribute to the extensive "hybrid zone." Hybridization, even at species and subspecies levels, may result in the virtual disappearance of pure native forms, but the introduced species and the hybrids registered a reduced growth rate compared to natives.
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Hemophilia
D. Nance, in Brenner's Encyclopedia of Genetics (Second Edition), 2013
Factor VIII Gene (F8)
This gene is in chromosome band Xq28, 1.5 Mb from the telomere. It spans 186 kb, contains 26 exons, and is oriented so that the promoter lies telomeric to the rest of the gene. A CpG island in intron 22 of F8 is the origin of two nested genes: F8A and F8B. The first is a 1.8-kb intronless gene entirely contained within intron 22 and transcribed in opposite orientation to the factor VIII gene. The second is transcribed in the orientation of the factor VIII gene, and its message contains a specific first exon followed by exons 23 to 26 of the factor VIII gene. The CpG island at the origin of the F8A and F8B genes is part of a 9503 bp segment of intron 22 of the factor VIII gene called int22h that is found repeated in opposite orientation 350 and 450 kb telomeric to the factor VIII gene. These three repeats are designated int22h-1, -2, and -3 according to their increasing distance from the centromere; they are important in factor VIII mutations (see below). The F8 gene produces an mRNA of 9028 nucleotides (nt).
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Lysis of the Host by Bacteriophage
R.F. YoungIII, R.L. White, in Encyclopedia of Virology (Third Edition), 2008
Rz–Rz1 encodes the spanin complex
The most distal genes of the lambda lysis cassette, Rz and Rz1, have an unusual relationship in that the smaller gene, Rz1, is entirely embedded within Rz in the +1 reading frame. Although there are a few other examples of such out-of-frame nested genes (see below for two examples in other phage lysis systems), Rz and Rz1 are unique in biology because the two genes are required for the same biological function. The products of the two reading frames are components of a complex that spans the entire periplasm, from the cytoplasmic membrane to the outer membrane (OM). This function of this complex is unknown, but it appears to be important for efficient disruption of the envelope. The evidence for this is that, in the absence of either Rz or Rz1, lysis is blocked if the OM is stabilized by ∼10 mM divalent cations in the medium. The terminal phenotype is a mechanically fragile spherical cell, presumably bounded by the stabilized OM.
Rz–Rz1 equivalents are found in almost all phages of Gram-negative bacteria. The genes are highly diverse, both in terms of sequence and gene arrangement. In many cases, the Rz1 gene begins within the Rz gene but extends beyond its end. In other cases, the Rz and Rz1 genes are completely separated, although always in the order Rz–Rz1. Rz proteins are type II 'signal anchor' proteins, with an N-terminal TMD tethering a periplasmic domain to the bilayer. Rz1 proteins are lipoproteins that are attached to the inner surface of the OM by the lipid and fatty acid groups of the modified N-terminal Cys residue. Rz and Rz1 form complexes by a specific C-terminal interaction. In the classic coliphage T1, the Rz–Rz1 genes are replaced by a single gene encoding a larger OM lipoprotein with the unique feature of a C-terminal TMD. Because this lipoprotein spans the entire envelope, it has been designated as a 'spanin'. The more common Rz–Rz1 pairs comprise a functional equivalent to the spanin, albeit with different topology.
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Synapsins
M.V. Khvotchev, J. Sun, in Encyclopedia of Neuroscience, 2009
Structure of Synapsins
Synapsins are an evolutionary conserved protein family found in most species throughout the animal kingdom, ranging from Caenorhabditis elegans to humans. In invertebrates, a single gene for synapsin has been identified. Most vertebrate species contain three synapsin genes, termed I, II, and III. Each synapsin gene appears to include a nested gene for tissue inhibitor of metalloproteinases.
The mRNAs transcribed from synapsin genes are alternatively spliced at the 3′ ends. In mammals, alternative splicing gives rise to two isoforms for each synapsin I and II: the long forms, called synapsins Ia and IIa, and the short forms, called synapsins Ib and IIb. For synapsin III, only the long IIIa isoform has been characterized. However, analysis of gene organization and mRNA transcripts in humans indicates that at least six different synapsin III isoforms may be present.
Sequence comparison reveals that all synapsins consist of an assortment of conserved and variable domains (Figure 1). The first 400 amino acids of all synapsins form three signature domains: a short conserved domain A; a variable domain B that is enriched in prolines, serines, and glycines; and a large highly conserved domain C. The C-terminal parts of synapsins are highly divergent and contain a variety of short domains from D to J (Figure 1). The only domain shared by all three synapsins in this area is domain E, found at the C-termini of synapsins Ia, IIa, and IIIa.

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Figure 1. Domain organization of the five synapsins. Domains are color coded and labeled on top. Amino acid residue scale is shown below.
The three-dimensional structure of the largest and most conserved domain in synapsins, domain C, has been determined (Figure 2). Domain C shows remarkable structural similarity to a family of bacterial ligases and synthetases, suggesting that synapsins may be adenosine triphosphate (ATP)-utilizing enzymes.

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Figure 2. Ribbon diagram of the complex of the rat synapsin I domain C complexed with ATP and calcium (PDB entry 1PX2).
All synapsins contain several conserved and isoform-specific phosphorylation consensus sites for multiple protein kinases. Domain A in all synapsins carries a phosphorylation site for protein kinase A (PKA) and CaM kinase I/IV. Domain C contains a single conserved site for tyrosine kinase Src. In addition, domains B and D in synapsin I contain multiple sites for MAPK, cdk1, cdk5, and CaMK II kinases.
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Nested Gene
A gene is defined biochemically as that segment of DNA (or in a few cases RNA) that encodes the information required to produce functional biological products.
From: Bio-Based Polymers and Composites, 2005
Related terms:
Allele
MicroRNA
Apoptosis
Phenotype
Mutation
Gene Expression
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Genes
Marcus Pembrey, in Genetic and Metabolic Disease in Pediatrics, 1985
THE STRUCTURE AND FUNCTION OF GENES
The genetic code and translation
A working definition of a gene will emerge during this section but, in essence, it is that part of the DNA double helix within the chromosome that codes for a single RNA molecule that in turn usually dictates the synthesis of a polypeptide at a ribosome in the cell cytoplasm. It will be recalled that DNA consists of two strands, each with a sugar–phosphate backbone and a linear array of any combination of the four nucleotide bases, adenine (A), guanine (G), cytosine (C) and thymine (T). The two DNA strands are held together by the complementary nature of the nucleotide base sequences; adenine only pairs with thymine, and guanine with cytosine (Watson and Crick, 1953). When transcription takes place one of the two DNA strands acts as a template for the formation of an RNA molecule that will have a complementary base sequence. The only difference is that RNA has uracil (U) instead of thymine. The genetic code consists of a series of codons or base triplets, and as there are four different bases there are 64 combinations of three. Every codon except three codes for one of the 20 amino acids: UAA, UAG and UGA code for the termination of translation of the messenger RNA (mRNA) into a polypeptide chain (Crick et al., 1961; Watson, 1965). AUG is the codon for methionine, but also has the role of initiating translation of mRNA (Darnbrough et al., 1973; Schreier and Staehelin, 1973).
Once in the cytoplasm the mRNA associates with one or more ribosomes which allow amino acids to be assembled into polypeptide chains in accordance with genetic code of that particular mRNA. Translation is achieved with the support of other intermediary molecules called transfer RNA (tRNA) (Rich and Kim, 1978). These molecules bind an amino acid at one end, while the other end is capable of recognizing the mRNA codon for that particular amino acid (Schimmel and Söll, 1979). Initiation of translation is a complex process in which the mRNA binds to a ribosome together with the initiation tRNA, the whole process being facilitated by the temporary involvement of proteins called initiation factors (Hunt, 1980). Defects in the translation process itself (as opposed to the faithful translation of wrong messages) have not as yet been shown to be a feature of monogenic disease. It has been known for a long time that even the mRNA molecule in the cytoplasm is considerably longer than the sequence from initiation codon to termination codon corresponding to the polypeptide chain and, as will be seen inFigure 2.1, the unprocessed product of transcription of a gene, the primary transcript, is longer still.

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Figure 2.1. Schematic representation of the β-globin gene and the way it is transcribed into nuclear RNA which is then processed by addition of a CAP structure at the 5′ end and a polyadenyl tail at the 3′ end, and the removal of intervening sequences (IVS I and IVS II), before passing into the cytoplasm as messenger RNA. The position of codons 1 (corresponding to the first amino acid of the β chain), 30, 31, 104, 105 and 146, plus the initiation and termination codons, are indicated
Before turning our attention to the DNA it is worth clarifying the current system for writing nucleotide sequences. Since DNA is double-stranded, the codon CTC, for example, has a complementary codon GAG, which also corresponds to the mRNA codon, in this case for glutamic acid. Increasingly, the mRNA codon is used even when referring to DNA to save the reader doing mental transcription all the time.
Coding sequences and the organization of genes
In essence, each chromosome is a long DNA double helix molecule coiled and supercoiled and associated with clusters of histone molecules to form nucleosomes at regular intervals (Kornberg and Klug, 1981). Although the packing of DNA clearly has a great influence on whether a sequence is available for transcription, and therefore plays an important role in overall gene activity, this need not concern us when discussing the structure of individual genes. The overall length of genomic DNA in a single human nucleus (the diploid chromosome complement) is about 6000000000 base pairs (bp). The smaller genes such as those for α and β-globin, or insulin, are about 1000 bp or 1 kilobase (kb) in length and so there is an enormous difference in scale between genes and chromosomes, as illustrated in Figure 2.2. It is not surprising that the smaller genes were studied first, and this may have biased our view of gene size. The gene for the enzyme phenylalanine hydroxylase appears to be of the order of 100 kb (Woo, personal communication) and that for the coagulant factor, FVIII:C, is 186 kb (Gitchier et al., 1984).

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Figure 2.2. Schematic representation of chromosome 11 showing the relative size of a chromosome band, the β-globin cluster of genes and the β-globin gene. Recent evidence suggests the β-globin locus may be closer to the tip of the short arm, but data are conflicting
While a gene contains all the coding sequences necessary to dictate the synthesis of the appropriate polypeptide, it would be quite wrong to regard human genomic DNA as just the coding sequences of the different genes strung end to end. Only about 3–5% of DNA is coding sequences for proteins, there being an estimated 50000 such 'expressed' genes per haploid set of chromosomes (excluding those that code for ribosomal and transfer RNA). Thus the individual genes are separated by long stretches of intergenic DNA which is not transcribed, the exact function of which still requires elucidation. We do know, however, that most of the intergenic DNA consists of repetitive sequences, so called because the same sequence is repeated again and again throughout the genome. Intergenic DNA also contains regions that are called pseudogenes because they have very similar sequences to neighbouring genes, but appear to be inactive and could well be evolutionary remnants of genes that duplicated (Jeffreys, 1981). The finding that genes are separated by intergenic DNA was more or less expected, unlike the remarkable discovery in 1977 (Breathnach, Mandel and Chambon, 1977; Doel et al., 1977) that the genes themselves are split up into separate regions. On the evidence so far it seems that, with very rare exceptions, human genes have their coding sequences (exons) interrupted by one or more non-coding regions called intervening sequences, or introns. Comparison of the intervening sequences in the globin genes of different animals shows that the number and their relative position tend to be conserved during evolution (Jeffreys, 1981). Certainly the actual base sequence around the junctions at the start and end of introns is critical for appropriate processing of the primary transcript (Chambon, 1981), as illustrated well by the mutations at these junctions, described later.
Figure 2.1 shows the overall arrangement of the β-globin gene (Lawn et al., 1980). The whole coding sequence is split into three exons by two introns. There is some flanking DNA at either end which is an integral part of the gene because it dictates the structure of the non-coding parts of the messenger RNA. Interference with the normal functioning of a gene can result from a mutation or change in DNA sequence in the coding sequences, the intervening sequence or in the flanking DNA at either end; and therefore for practical purposes it is appropriate to define a gene as the length of DNA that contains all these elements plus some additional untranscribed sequences upstream that are required for the start of transcription. We know so little about the function of DNA sequences that are not normally transcribed that inclusion of these in the definition, even if they are unique sequences, is unhelpful.
Regulation of gene transcription
The regulation of gene activity is still poorly understood, but once the transcription is started the chain of events essentially follows the pattern in Figure 2.1. Transcription itself requires the action of a family of enzymes called RNA polymerases, one type of which, RNA polymerase II, is involved in the synthesis of RNA that will be translated into a protein. Obviously there has to be some signal to indicate exactly where transcription should start, and there is increasing evidence of certain DNA sequences upstream of the sequences to be transcribed acting as recognition sites for RNA polymerase (Corden et al., 1980; Breathnach and Chambon, 1981). One such sequence, the so-called CCAAT box, is found about 70 bp upstream, and another, the TATA box, is usually found closer to the start site for transcription. Transcription is not initiated whenever these sequences occur in the genome, but when they and other sequences often within the gene are all in the appropriate positions.
In addition to sequences essential for transcription, there are other sequences that can modulate the rate of transcription. Karin et al. (1984) have recently characterized the DNA sequences, or genetic elements, through which cadmium and glucocorticoid hormones can induce (i.e. increase the active transcription of) the human metallothionein-II gene. Metallothionein (MT) genes encode heavy-metal binding proteins, and administration of heavy-metal ions or glucocorticoid hormones to cells can stimulate increased transcription of the MT gene. The genetic element for steroid induction is a 25 bp sequence 250 bases upstream from the start of the transcribed portion. Interestingly, it turns out to be the DNA-binding site for the glucocorticoid hormone-receptor complex. There are going to be an increasing number of similar examples in the future, from which will emerge some clearer picture of how short term modulation of gene activity operates (see Perry, 1984).
RNA processing
Figure 2.1 illustrates how all the coding sequences, intervening sequences and flanking sequences at either end are initially transcribed into a huge precursor molecule called heterogeneous nuclear RNA. This primary transcript is first modified at the 5′ end to form a structure called CAP (Perry, 1981), and also has a string of adenyl acid residues added to the 3′ end to form a poly-A tail (Lim and Canellakis, 1970). All mRNA molecules are capped and tailed in this way, and it seems that the CAP is involved in the initiation of mRNA translation and the poly-A tail with the stability of the molecule in the cytoplasm (Breathnach and Chambon, 1981). There next follows a very precise splicing together of the coding sequences during which the intervening sequences are excised.Figure 2.8 (p. 21) illustrates what is thought to be one mechanism where molecules such as U-1 RNA can play a part in holding the exons to be joined together in the correct alignment (Lerner and Steitz, 1981). It is likely that the RNA molecule cannot leave the nucleus until the intervening sequences have been spliced out and the coding regions for the polypeptide chain brought together as a continuous sequence.
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Figure 2.8. (a) A diagram showing the normal and abnormal processing of the nuclear RNA for β-globin in one form of β+-thalassaemia. (b) The nucleotide sequence around the splice junctions for the IVS I of β-globin nuclear RNA, and how the G→A mutation in the IVS I creates a new splice junction and abnormal splicing
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Gene
Javad Parvizi MD, FRCS, ... Associate Editor, in High Yield Orthopaedics, 2010
Inheritance:
•
Majority dictated by Mendelian modes
•
Each has two alleles (form of gene), which may be dominant or recessive
•
Autosomal dominant
•
Only one disease-associated allele required
•
Results in structural deficiency
Fig. 99-1.
(Adapted from Rosenthal N: Regulation of gene expression. N Engl J Med 331:931–932, 1994; From Abeloff M: Abeloff's Clinical Oncology, 4th ed. Philadelphia, Churchill Livingstone, 2008.)
•
Autosomal recessive
•
Two disease-associated alleles required
•
Results in enzymatic deficiency
•
X-Linked dominant: Only one disease-associated allele specifically on the X chromosome required
•
X-Linked dominant: Requires either two disease-carrying X chromosomes in a female or more likely the mother's in a son
Table 99-1.. MODES OF INHERITANCE
Autosomal DominantAutosomal RecessiveX-Linked DominantX-Linked RecessiveAchondroplasiaDiastrophic dysplasiaHypophosphatemic ricketsBecker's dystrophyCharcot-Marie-ToothFriedreich's ataxiaDuchenne's muscular dystrophy
Hunter's syndromeDupuytren's contracture
Ehlers-Danlos
Kniest's dysplasia
Limb-girdle muscular dystrophyHereditary vitamin D–dependent rickets
Hurler's syndrome
Hypophosphatasia
Laron's dysplasiaMarfan syndromeOsteogenesis imperfecta (II and III)Metaphyseal chondrodysplasiaSickle cellOsteochondromatosisSpinal muscular atrophyOsteogenesis imperfecta (I and IV)
Osteopetrosis
Polydactyly
Non-Mendelian: Ewings sarcoma, Albrights hereditary osteodystrophy, scoliosis, Osgood-Schlatter, slipped capital femoral epiphysis.
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Evolution of Life on Earth
In Cell Biology (Third Edition), 2017
Genes with a common ancestor are homologs. The terms ortholog and paralog describe the relationship of homologous genes in terms of how their most recent common ancestor was separated. If a speciation event separated two genes, then they are orthologs. If a duplication event separated two genes, then they are paralogs. To illustrate this point, let us say that gene A is duplicated within a species, forming paralogous genes A1 and A2. If these genes are separated by a speciation event, so that species 1 has genes sp1A1 and sp1A2 and species 2 has genes sp2A1 and sp2A2, it is proper to say that genes sp1A1 and sp2A1 are orthologs and genes sp1A1 and sp1A2 are paralogs, but genes sp1A1 and sp2A2 are also paralogs because their most recent common ancestor was the gene that duplicated.
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Basic Genetics
David P. Clark, ... Michelle R. McGehee, in Molecular Biology (Third Edition), 2019
4 Phenotypes and Genotypes
In real life, most biochemical pathways have several steps, not just one. To illustrate this, extend the pathway that makes red pigment so it has three steps and three genes, called A, B, and C. If any of these three genes is defective, the corresponding enzyme will be missing, the red pigment will not be made, and the flowers will be white. Thus, mutations in any of the three genes will have the same effect on the outward appearance of the flowers. All three genes must be intact for the pathway to succeed in making its final product. (Fig. 2.04).

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Figure 2.04. Three-Step Biochemical Pathway
In this scenario, genes A, B, and C are all needed to make the red pigment required to produce a red flower. If any precursor is missing due to a defective gene, the pigment will not be made and the flower will be white.
Outward characteristics—the flower color—are referred to as the phenotype and the genetic make-up as the genotype. Obviously, the phenotype "white flowers" may be due to several possible genotypes, including defects in gene A, B, or C, or in genes not mentioned here that are responsible for producing precursor P in the first place, or even in genes responsible for the deposition of pigment into the petals. If white flowers are seen, only further analysis will show which gene or genes are defective. This might involve assaying the biochemical reactions, measuring the build-up of pathway intermediates (such as P or Q in the example) or mapping the genetic defects to locate them in a particular gene(s).
If gene A is defective, it no longer matters whether gene B or gene C are functional (at least as far as production of our red pigment is concerned; some genes affect multiple pathways, a possibility not considered in this analysis). A defect near the beginning of a pathway will make the later reactions irrelevant. This is known in genetic terminology as epistasis. Gene A is epistatic to gene B and gene C; that is, it masks the effects of these genes. Similarly, gene B is epistatic to gene C. From a practical viewpoint, this means that a researcher cannot tell if genes B or C are defective or not, when there is already a defect in gene A.
Remember that phenotypes refer to physical traits, and genotypes refer to the genes that confer the trait.
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Reg Proteins and Their Roles in Inflammation and Cancer of the Human Digestive System
Jie Zhao, ... Maode Lai, in Advances in Clinical Chemistry, 2013
3.2.3 Cancer cell growth and metastasis
Reg protein is expressed in many types of gastric cancer cells and induces their proliferation. Fukui et al. found that one-third of gastric cancer tissue samples are positive for Reg1 protein, and Reg1-positive gastric cancers show a significantly higher proliferating cell nuclear antigen labeling index than negative cancers. This indicates that Reg enhances the proliferation of gastric cancer [65].
Moreover, Reg proteins participate in the invasive and metastatic process. Reg1 correlates positively with lymphatic and venous invasion [57,65], and Reg4 induces peritoneal metastasis in mice and patients with gastric cancer [66–68].
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Resistance of the Race-Specific Type
P.L. Dyck, E.R. Kerber, in Diseases, Distribution, Epidemiology, and Control, 1985
C INHIBITORY EFFECTS
Genes conditioning host resistance can also be inhibited or suppressed by nonallelic genes. The resistance to Canadian leaf rust cultures conferred by gene Lr23 is suppressed by a gene in Thatcher, but this suppression is only partially effective with Australian cultures (McIntosh and Dyck, 1975). Kerber and Green (1980) observed that Canthatch nullisomic 7D is much more resistant to several cultures of stem rust than normal disomic Canthatch. They concluded that chromosome 7DL carries a gene that inhibits the expression of one or more genes for rust resistance present on other chromosomes of Canthatch.
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Pediatric Neurology Part III
Brigitte Chabrol, ... Berge Minassian, in Handbook of Clinical Neurology, 2013
Other genes
Novel genes have recently been involved in NCL (Anderson et al., 2013). Mutations have been found in the potassium channel related gene KCTD7 or CLN14 gene in patients of different origin, presenting with early-onset progressive myoclonic epilepsy. Some patients with juvenile NCL have mutations in the ATP13A2 or CLN12 gene. In the autosomal recessive adult forms of NCL, mutations have been reported either in the progranulin gene (GRN or CLN11 gene) or in the cathepsin F gene (CTSF or CLN13 gene). Some patients with autosomal dominant form called Parry disease, differing by the absence of myoclonus epilepsy and ataxia, have mutations in the DNAJC5 or CLN4 gene encoding a cysteine-string protein alpha.
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The Role of TCP Transcription Factors in Shaping Flower Structure, Leaf Morphology, and Plant Architecture
Michael Nicolas, Pilar Cubas, in Plant Transcription Factors, 2016
TCP Genes and the Control of Leaf Development 250
16.2.1
TCP Genes and the Development of Simple Leaves 250
16.2.1.1
CIN Genes and Simple Leaf Development 250
16.2.1.2
CYC/TB1 Genes and Simple Leaf Development 252
16.2.1.3
Class I TCP and Simple Leaf Development 252
16.2.2
Role of TCP Genes During Compound Leaf Development 253
16.2.3
TCP-Regulated Networks in the Control of Leaf Development 253
16.2.3.1
TCP Regulation of the CUC/KNOX1 Gene Pathway 253
16.2.3.2
TCP Regulation of Growth-Regulating Factors 254
16.2.3.3
TCP Regulation of Auxin Signaling During Leaf Development 255
16.2.3.4
TCP Regulation of CK Signaling During Leaf Development 255
16.2.3.5
TCP Genes and Gibberellin Signaling 255
16.2.3.6
TCP Genes and Jasmonate Signaling 256
16.2.4
Posttranslational Regulation of TCP Genes During Leaf Development 256
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Genetic Nomenclature, Mouse☆
T. Floss, J. Guimera, in Reference Module in Life Sciences, 2017
Gene Trap Loci
Gene trap experiments in embryonic stem (ES) cells produce cell lines in which a reporter gene is integrated into an endogenous locus. The integration of the gene trap vector may mutate or affect the expression of a gene in different ways, which each of them may display different phenotypes usually (though not necessarily), depending on the site of integration. Series of different gene trap alleles are characterized by the prefix "Gt" (for gene trap), followed by a vector designation parenthetically, a serial number assigned by the laboratory characterizing the locus, and the laboratory code (typically three to four letters with the first uppercase) that identifies the investigator or Institute that discovered or produce of a locus.
Examples:
Gt(ROSA)26Sor
A gene trap clone where the integration site is unknown; Philippe Soriano.
Ntn1Gt(ROSA)26Sor
Full allele designation once it is known that the integration site is in the Ntn1 gene
Sall4Gt(W097E01)Flo
Sal-like 4 locus; gene trap W097E01; Thomas Floss
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