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Results for “genomic tandem array”

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PubMed2000

A novel interspersed type of organization of satellite DNAs in Tribolium madens heterochromatin.

Analysis of arrangement of satellite DNA sequences in Tribolium madens (Insecta, Coleoptera) by Southern analysis of pulsed-field blots and two colour FISH on extended chromosomes and DNA fibres revealed a novel type of heterochromatin organization. Two satellite DNAs, distributed over the whole pericentromeric heterochromatin of all chromosomes form clusters, ranging in size from 150 kb up to several Mb. Within the clusters, both satellites are in the form of highly interspersed, short homogeneous arrays which vary in size with a lowest length limit of only few kb. The longest arrays composed of a single satellite are relatively short, up to 70 kb for satellite I, and up to 45 kb for satellite II. Only a small fraction of about 15% of satellite II is organized in long tandem repeats, while the rest is in the form of only a few repeats intermingled with satellite I. The results indicate that large clusters composed of interspersed arrays of both satellites represent a major component of T. madens heterochromatin, which is mostly devoid of long regions of other sequences. The same organizational pattern probably also includes a region of the functional centromere. We propose that such an organizational pattern of DNA sequences in heterochromatin might be common in genomes characterized by a high rate of interchromosomal exchange. This pattern of organization is different from that in other animal as well as plant species analysed up to now, in which every satellite in heterochromatin is organized in a small number of large separate domains.

Animals↗

PubMed1978

Genetic organization of the ribosomal transcription units of the yeast Saccharomyces carlsbergensis.

The genetic organization of the multiple ribosomal transcription units (RTUs) on the genome of the yeast Saccharomyces carlsbergensis was studied by electron microscopy of purified ribosomal DNA hybridized to 26S rRNA using the R-loop technique (Thomas, M., White, R.L. and Davis, R.W. (1973) Proc. Natl. Acad. Sci. U.S. 73, 2294-2298). Plasmid pBR 322, the molecular weight of which is known, was used as a standard for converting contour length of double-stranded DNA into molecular weight. The 140 yeast RTUs were found to be arrayed in tandem repeats, each repeat containing at most 0.4 X 10(6) D (about 6% of the length of the RTU) of non-transcribed spacer DNA. The repeats, in turn, are arranged in a number of clusters separated by much longer stretches of non-ribosomal DNA.

Genes↗

PubMed2002

Ancient lineages of non-LTR retrotransposons in the primitive eukaryote, Giardia lamblia.

Mobile elements that use reverse transcriptase to make new copies of themselves are found in all major lineages of eukaryotes. The non-long terminal repeat (non-LTR) retrotransposons have been suggested to be the oldest of these eukaryotic elements. Phylogenetic analysis of non-LTR elements suggests that they have predominantly undergone vertical transmission, as opposed to the frequent horizontal transmissions found for other mobile elements. One prediction of this vertical model of inheritance is that the oldest lineages of eukaryotes should exclusively harbor the oldest lineages of non-LTR retrotransposons. Here we characterize the non-LTR retrotransposons present in one of the most primitive eukaryotes, the diplomonad Giardia lamblia. Two families of elements were detected in the WB isolate of G. lamblia currently being used for the genome sequencing project. These elements are clearly distinct from all other previously described non-LTR lineages. Phylogenetic analysis indicates that these Genie elements (for Giardia early non-LTR insertion element) are among the oldest known lineages of non-LTR elements consistent with strict vertical descent. Genie elements encode a single open reading frame with a carboxyl terminal endonuclease domain. Genie 1 is site specific, as seven to eight copies are present in a single tandem array of a 771-bp repeat near the telomere of one chromosome. The function of this repeat is not known. One additional, highly divergent, element within the Genie 1 lineage is not located in this tandem array but is near a second telomere. Four different telomere addition sites could be identified within or near the Genie elements on each of these chromosomes. The second lineage of non-LTR elements, Genie 2, is composed of about 10 degenerate copies. Genie 2 elements do not appear to be site specific in their insertion. An unusual aspect of Genie 2 is that all copies contain inverted repeats up to 172 bp in length.

Animals↗

PubMed2003

Genesis of variants of Vibrio cholerae O1 biotype El Tor: role of the CTXphi array and its position in the genome.

The gene encoding cholera toxin, the principal virulence factor of Vibrio cholerae, is encoded by a filamentous, lysogenic bacteriophage known as CTXphi. The genome of V. cholerae, the host for CTXphi, consists of two chromosomes, one large and one small. Here, it is shown that localization and array of CTX prophage DNA in either the large or small chromosome of V. cholerae is likely to be one of the reasons for the emergence of O1 biotype El Tor variants isolated just before and after the V. cholerae O139 cholera outbreak in 1992. Analyses of the organization of the CTX region of the genome of pre-O139 El Tor strains revealed that these strains carry two distinct CTX prophages integrated in the small chromosome in tandem: CTX(ET), the prophage having a conserved NotI site in its repeat sequence segment which seems to be specific for the El Tor strains so far examined, followed by CTX(calc)-like genome, the prophage found in recent O139 clinical isolates from Calcutta. In sharp contrast, in post-O139 El Tor strains only one copy of the CTX(ET) prophage was found to be integrated in the large chromosome. To the authors' knowledge, the presence of CTX prophage in the small chromosome of O1 El Tor strains has not been reported previously. It is also shown that the difference in the CTX copy number and the position of the bacteriophage on the genomes of pre- and post-O139 El Tor strains have an effect on cholera toxin production. While a pre-O139 strain produced maximum cholera toxin in yeast extract/peptone medium at 30 degrees C, a post-O139 El Tor strain showed maximal yield at 37 degrees C, indicating differential regulation of cholera toxin between the strains. It appears from this study that the variation in the integration site of the CTX prophage, its copy number and the presence of diverse phage genomes in V. cholerae O1 biotype El Tor may be strategically important for generating variants with subtle phenotypic modulations of virulence factor production in this longest-ruling seventh pandemic strain.

Bacteriophages↗

PubMed2006

Unique posttranslational modifications of chitin-binding lectins of Entamoeba invadens cyst walls.

Entamoeba histolytica, which causes amebic dysentery and liver abscesses, is spread via chitin-walled cysts. The most abundant protein in the cyst wall of Entamoeba invadens, a model for amebic encystation, is a lectin called EiJacob1. EiJacob1 has five tandemly arrayed, six-Cys chitin-binding domains separated by low-complexity Ser- and Thr-rich spacers. E. histolytica also has numerous predicted Jessie lectins and chitinases, which contain a single, N-terminal eight-Cys chitin-binding domain. We hypothesized that E. invadens cyst walls are composed entirely of proteins with six-Cys or eight-Cys chitin-binding domains and that some of these proteins contain sugars. E. invadens genomic sequences predicted seven Jacob lectins, five Jessie lectins, and three chitinases. Reverse transcription-PCR analysis showed that mRNAs encoding Jacobs, Jessies, and chitinases are increased during E. invadens encystation, while mass spectrometry showed that the cyst wall is composed of an approximately 30:70 mix of Jacob lectins (cross-linking proteins) and Jessie and chitinase lectins (possible enzymes). Three Jacob lectins were cleaved prior to Lys at conserved sites (e.g., TPSVDK) in the Ser- and Thr-rich spacers between chitin-binding domains. A model peptide was cleaved at the same site by papain and E. invadens Cys proteases, suggesting that the latter cleave Jacob lectins in vivo. Some Jacob lectins had O-phosphodiester-linked carbohydrates, which were one to seven hexoses long and had deoxysugars at reducing ends. We concluded that the major protein components of the E. invadens cyst wall all contain chitin-binding domains (chitinases, Jessie lectins, and Jacob lectins) and that the Jacob lectins are differentially modified by site-specific Cys proteases and O-phosphodiester-linked glycans.

Amino Acid Sequence↗

PubMed1991

Genetic instability and associated genome plasticity in Streptomyces ambofaciens: pulsed-field gel electrophoresis evidence for large DNA alterations in a limited genomic region.

Using pulsed-field gel electrophoresis (PFGE) analysis, the amplifiable units of DNA (AUD) loci AUD6 and AUD90 of Streptomyces ambofaciens DSM40697 could be mapped in the wild-type genome within two adjacent AseI restriction fragments estimated to be about 75 and 850 kb. In addition, the genetic instability and formation of very large deletions were strictly correlated. Their sizes were estimated to range from 250 to more than 2,000 kb. These deletions affected the DNA region overlapping both amplifiable loci. PFGE also allowed us to localize the amplified DNA sequences and to establish their structure: amplification takes place at the AUD locus as a tandem array of the wild-type AUD sequence.

DNA, Bacterial↗

PubMed1994

Genetic determination of telomere size in humans: a twin study of three age groups.

Reduction of telomere length has been postulated to be a causal factor in cellular aging. Human telomeres terminate in tandemly arranged repeat arrays consisting of the (TTAGGG) motif. The length of these arrays in cells from human mitotic tissues is inversely related to the age of the donor, indicating telomere reduction with age. In addition to telomere length differences between different age cohorts, considerable variation is present among individuals of the same age. To investigate whether this variation can be ascribed to genetic influences, we have measured the size of terminal restriction fragments (TRFs) in HaeIII-digested genomic DNA from 123 human MZ and DZ twin pairs 2-95 years of age. The average rate of telomere shortening was 31 bp/year, which is similar to that observed by others. Statistical analysis in 115 pairs 2-63 years of age indicates a 78% heritability for mean TRF length in this age cohort. The individual differences in mean TRF length in blood, therefore, seem to a large extent to be genetically determined.

Adolescent↗

PubMed2000

Identification of brain-specific and imprinted small nucleolar RNA genes exhibiting an unusual genomic organization.

We have identified three C/D-box small nucleolar RNAs (snoRNAs) and one H/ACA-box snoRNA in mouse and human. In mice, all four snoRNAs (MBII-13, MBII-52, MBII-85, and MBI-36) are exclusively expressed in the brain, unlike all other known snoRNAs. Two of the human RNA orthologues (HBII-52 and HBI-36) share this expression pattern, and the remainder, HBII-13 and HBII-85, are prevalently expressed in that tissue. In mice and humans, the brain-specific H/ACA box snoRNA (MBI-36 and HBI-36, respectively) is intron-encoded in the brain-specific serotonin 2C receptor gene. The three human C/D box snoRNAs map to chromosome 15q11-q13, within a region implicated in the Prader-Willi syndrome (PWS), which is a neurogenetic disease resulting from a deficiency of paternal gene expression. Unlike other C/D box snoRNAs, two snoRNAs, HBII-52 and HBII-85, are encoded in a tandemly repeated array of 47 or 24 units, respectively. In mouse the homologue of HBII-52 is processed from intronic portions of the tandem repeats. Interestingly, these snoRNAs were absent from the cortex of a patient with PWS and from a PWS mouse model, demonstrating their paternal imprinting status and pointing to their potential role in the etiology of PWS. Despite displaying hallmarks of the two families of ubiquitous snoRNAs that guide 2'-O-ribose methylation and pseudouridylation of rRNA, respectively, they lack any telltale rRNA complementarity. Instead, brain-specific C/D box snoRNA HBII-52 has an 18-nt phylogenetically conserved complementarity to a critical segment of serotonin 2C receptor mRNA, pointing to a potential role in the processing of this mRNA.

Animals↗

PubMed2004

Use of genome level-informed PCR as a new investigational approach for analysis of outbreak-associated Mycobacterium tuberculosis isolates.

Mycobacterium tuberculosis strain CH, the index isolate linked to a major tuberculosis outbreak associated with high levels of transmissibility and virulence, was characterized by microarray analysis by use of a PCR product array representative of the genome of M. tuberculosis strain H37Rv. Seven potential genomic deletions were identified in CH, five of which were confirmed by PCR analysis across the predicted deletion points. The panel of five PCRs required to individually interrogate these loci was collectively referred to as the genome level-informed PCR (GLIP) assay. GLIP analysis was performed with CH, 12 other epidemiologically linked isolates, and 43 recent, non-outbreak-associated isolates derived from patients within the local area. All 13 outbreak-linked isolates showed a profile corresponding to the presence of all five deletions. These 13 isolates were also found to share common variable-number tandem repeat and mycobacterial interspersed repetitive unit profiles. None of the 43 non-outbreak-associated isolates exhibited the five-deletion profile. Although three individual deletions were present in upwards of 44% of the non-outbreak-associated isolates, no single-deletion isolates were detected. Interestingly, none of these deletions had been previously recognized, and sequence analysis of the immediate flanking regions in CH failed to identify a likely mechanism of deletion for four of the five loci. The GLIP assay also proved valuable in ongoing surveillance of the outbreak, rapidly identifying a further two outbreak-associated cases months after the initial cluster and, importantly, dismissing a further 12 epidemiologically suspect cases, which allowed the optimum deployment of public health resources.

Base Sequence↗

PubMed2003

Does chromosome 22 have anything to do with sex determination: further studies on a 46,XX,22q11.2 del male.

Several years ago, we presented a patient with true hermaphroditism and partial duplication of chromosome 22 and no evidence of SRY (Aleck et al. [1999: Am J Med Genet 85:2-4]). Recently a 46,XX male with velocardiofacial syndrome and a deletion of 22q11.2 and no evidence of Y chromosomal loci in blood DNA was reported (Phelan et al. [2003: Am J Med Genet 116A:77-79]). We have restudied this patient as he enters puberty. Because chromosomal deletions sometimes involve micro rearrangements of nearby material, we have extensively studied this individual's chromosome 22 looking for evidence of any gene duplication. We studied a number of variable number tandem repeat (VNTR) loci along chromosome 22 in the patient and both parents. Normal Mendelian inheritance of the VNTRs was found. We then used quantitative multiplex PCR of short fluorescent fragments (QMPSF) to delineate the 22q11.2 deletion in this patient (Jacquet et al. [2002: Hum Molec Genet 11:2243-2249]) and found a pattern of deletion typical of the velocardiofacial DiGeorge syndrome. Finally, the patient's DNA has been analyzed using a full coverage human chromosome 22 genomic microarray (array comparative genomic hybridization [CGH]) for evidence of rearrangements outside the classical velocardiofacial DiGeorge associated deletion (Buckley et al. [2002: Hum Molec Genet 11:3221-3229]). The array-CGH profile of this patient confirms the deletion encompassing the typically deleted region associated with the velocardiofacial DiGeorge syndrome and provides no support for additional gene copy number aberrations on 22q. Thus, there is no evidence of any chromosome 22 trisomic material. In this case, the rare events of sex reversal and 22q11.2 deletion may have occurred together by chance.

Chromosome Deletion↗

PubMedDate not supplied

Human genes for U2 small nuclear RNA map to a major adenovirus 12 modification site on chromosome 17.

U2 RNA is one of the abundant, highly conserved species of small nuclear RNA (snRNA) molecules implicated in RNA processing. As is typical of mammalian snRNAs, human U1 and U2 are each encoded by a multigene family. In the human genome, defective copies of the genes (pseudogenes) far outnumber the authentic genes. The majority or all of the 35 to 100 bona fide U1 genes have at least 20 kilobases (kb) of nearly perfect 5' and 3' flanking homology in common with each other; these U1 genes are clustered loosely in chromosome band 1p36 (refs 5, 7) with intergenic distances exceeding 44 kb. In contrast, the 10 to 20 U2 genes are clustered tightly in a virtually perfect tandem array which has a strict 6-kb repeating unit. We report here the assignment, by in situ hybridization, of the U2 gene cluster to chromosome 17, bands q21-q22. Surprisingly, this region is one of three major adenovirus 12 modification sites which undergo chromosome decondensation ('uncoiling') in permissive human cells infected by highly oncogenic strains of adenovirus. The two other major modification sites, 1p36 and 1q21, coincide with the locations of U1 genes and class I U1 pseudogenes, respectively. We suggest that snRNA genes are the major targets of viral chromosome modification.

Adenoviruses, Human↗

PubMed1991

Chromosome structure: DNA nucleotide sequence elements of a subset of the minichromosomes of the protozoan Trypanosoma brucei.

The genome of the protozoan Trypanosoma brucei contains a set of about 100 minichromosomes of about 50 to 150 kb in size. The small size of these chromosomes, their involvement in antigenic variation, and their mitotic stability make them ideal candidates for a structural analysis of protozoan chromosomes and their telomeres. We show that a subset of the minichromosomes is composed predominantly of simple-sequence DNA, with over 90% of the length of the minichromosome consisting of a tandem array of 177-bp repeats, indicating that these molecules have limited protein-coding capacity. Proceeding from the tip of the telomere to a chromosome internal position, a subset of the minichromosomes contained the GGGTTA telomere repeat, a 29-bp telomere-derived repeat, a region containing 74-bp G + C-rich direct repeats separated by approximately 155 bp of A + T-rich DNA that has a bent character, and 50 to 150 kb of the 177-bp repeat. Several of the minichromosome-derived telomeres did not encode protein-coding genes, indicating that the repertoire of telomeric variant cell surface glycoprotein genes is restricted to some telomeres only. The telomere organization in trypanosomes shares striking similarities to the organization of telomeres and subtelomeres in humans, yeasts, and plasmodia. An electron microscopic analysis of the minichromosomes showed that they are linear molecules without abnormal structures in the main body of the chromosome. The structure of replicating molecules indicated that minichromosomes probably have a single bidirectional origin of replication located in the body of the chromosome. We propose a model for the structure of the trypanosome minichromosomes.

Animals↗

PubMed1985

A polymorphic repetitive-sequence PR1 family. Evidence for meiotic instability.

When EcoRI digests of mouse genomic DNA were subjected to Southern blot analysis with the polymorphic repetitive sequence PR1 as a probe, one satellite-like band of 3.5 X 10(3) base-pairs, designated as PR1 family B, was detected in BALB/c-strain mice, but not in the DDD/1- or MOA-strain mice. Analysis of recombinant phage clones revealed that the repeating unit of the PR1 family B was 13.5 X 10(3) base-pairs long. This family consisted of a tandem array of repeating units and occupied as much as 2% of one BALB/c chromosome. Since the BALB/c-specific PR1 family B is not present in DDD/1 or MOA mice, the unpaired portion of the BALB/c chromosome may be looped out in a synaptonemal complex during meiosis in F1 hybrids of the BALB/c strain with DDD/1 or MOA. To determine the fate of this extra DNA, we examined the genotypes of the F1 hybrid mice and of the segregating populations. Although the PR1 patterns of F1 and most N2 mice are consistent with typical Mendelian inheritance, some N2 progeny showed an abnormal 3.5 X 10(3) base-pair band of unexpectedly reduced intensity. This indicated that the extra DNA of PR1 family B occasionally underwent recombination during meiosis in F1 mice, resulting in its apparent excision. Examination of PstI digests supported this interpretation.

Animals↗

PubMed1994

Seripauperins of Saccharomyces cerevisiae: a new multigene family encoding serine-poor relatives of serine-rich proteins.

A gene, PAU1, has been cloned from Saccharomyces cerevisiae and sequenced. It is located in a telomeric region, probably on chromosome IV, and contains an open reading frame encoding a protein of 120 amino acids (aa) (approx. 13 kDa). The deduced sequence is nearly identical to two other genes found in GenBank (named PAU2 and PAU3 by us), which are located close to the ends of chromosomes V and III, respectively. Blotting of separated chromosomes with a PAU1 probe at high stringency revealed that at least six chromosomes in addition to III, IV and V possessed related sequences, suggesting a large gene family. Probing of an ordered array of phage lambda clones containing yeast genomic DNA inserts ('Olson filters') revealed ten additional hybridizing sequences, located close to the ends of the left and/or right arms of chromosomes I, II, VII, VIII, X, XII, XIV and XV. Transcription of these sequences could not be demonstrated, however, under a wide variety of growth and culture conditions. The deduced PAU1, PAU2 and PAU3 aa sequences are all highly homologous with the SRP1 aa sequences, which contains eight serine-rich tandem repeats of 12 aa each, at its C terminus. This homology is limited, however, to the N-terminal half of SRP1, and does not include the repeats. In fact, PAU1 is quite serine-poor (5.8%), leading to the suggested name of seripauperins for this family of genes.

Amino Acid Sequence↗

PubMed2026

The emergence and diversification of the DUX gene family across placental mammals.

The DUX gene family encodes transcription factors with paired homeodomains. It has critical roles in embryogenesis and disease, including facioscapulohumeral muscular dystrophy (FSHD) and cancer. This study conducts a comparative analysis of the DUX gene family-DUXA, DUXB (including DUXBL), and DUXC (including DUX4 and Dux)-across placental mammals, highlighting their structural diversity within macrosatellite repeat contexts. Using long-read genomes, we explore gene distribution, array patterns, and phylogenetic relationships in various vertebrate species. Our analysis reveals that DUXA and DUXB are highly conserved, with intriguing variations such as intronless forms likely arising from ancestral retrotransposition events. While DUXBL is inconsistently retained across clades, its locus-which in non-placental mammals harbors the ancestral single-homeodomain sDUX gene-served as an evolutionary hub for diversification, giving rise to DUXA, DUXB and DUXC, as well as macrosatellite tandem array structures. Sequence conservation and syntenic analyses demonstrate array adaptability, exemplified by higher-order repeats in orangutans and disrupted patterns of concerted evolution in elephants. Furthermore, analysis of human pseudo-DUX4 arrays indicates their potential role in disease mechanisms, including as possible contributors to rare cases of FSHD, warranting further investigation. This study thus provides insights into DUX-family gene evolution, offering a foundation for future research into developmental roles and disease implications.

Animals↗

PubMed1997

PilP, a pilus biogenesis lipoprotein in Neisseria gonorrhoeae, affects expression of PilQ as a high-molecular-mass multimer.

Studies of gonococcal pilus biogenesis are fundamental to understanding organelle structure/function relationships and identifying new approaches to controlling disease. This area of research is also relevant to elucidating the basic mechanisms of outer membrane translocation of macromolecules, which requires components highly related to those involved in type IV pilus expression. Previous studies have shown that products of several ancillary pil genes are required for organelle biogenesis but of these only PilQ, a member of the GspD protein family, is a component of the outer membrane. DNA sequencing of the region upstream of pilQ revealed the presence of two open reading frames (ORFs) whose deduced polypeptides shared significant identities with proteins required for pilus expression in Pseudomonas aeruginosa and Pseudomonas syringae, the genes for which are arrayed upstream of a gene encoding a PilQ homologue. Gonococcal mutants bearing transposon insertions in these ORFs were non-piliated and failed to express pilus-associated phenotypes, and the corresponding genes were designated PilO and pilP. The piliation defects in the mutants could not be ascribed to polarity on distal pilQ expression as shown by direct measurement of PilQ antigen in those backgrounds and the use of a novel technique to create tandem duplications in the gonococcus (Gc) genome. As predicted by the presence of a consensus lipoprotein signal sequence, PilP expressed in both Escherichia coli and Gc could be labelled with [3H]-palmitic acid. PilP- as well as PilQ- mutants shed PilC, a protein which facilitates pilus assembly and is implicated in epithelial cell adherence, in a soluble form. Combined with the finding that levels of multimerized PiIQ were greatly reduced in PilP- mutants, the results suggest that PilP is required for PilQ function and that PilQ and PilC may interact during the terminal stages of pilus biogenesis. The findings also support the hypothesis that the Gc PilQ multimer corresponds to a physiologically relevant form of the protein required for pilus biogenesis.

Bacterial Outer Membrane Proteins↗

PubMed1999

Elucidating sequence codes: three codes for evolution.

The sequences are related to evolution in several ways. First, they carry traces of a distant past. Two sequence features point to the earliest sequence organization. The universal hidden GCU-periodical pattern in mRNA suggests the earliest codons: GCU and its nine-point-change derivatives. They code for seven amino acids that by several criteria are also the oldest. Together it makes the earliest form of the triplet code, still recognizable in the extant sequences. Another feature present in the sequences, apparently, since separation of prokaryotes and eukaryotes, is hidden genome segmentation. Both protein-coding and noncoding sequences appear to have been formed by fusion of standard size units, about 360 bp (120 aa) in eukaryotes and 450 bp (150 aa) in prokaryotes. Presumably, the units have been functioning at some stage of evolution as autonomous single-gene size elements. There are sequence designs that promote evolution. One such design suitable for fast adaptation is the tandem repetition of identical sequences, so that their copy numbers in the repeat arrays would modulate (tune) the expression of nearby genes. The tandem repeat expansion diseases illustrate this mechanism in a dramatic way: overtuning of the respective gene expression leads to the disease.

Adaptation, Biological↗

PubMed1990

Molecular characterization of SerH3, a Tetrahymena thermophila gene encoding a temperature-regulated surface antigen.

The DNA sequences of a cDNA clone and the macronuclear genomic fragment corresponding to the functional copy of the SerH3 surface antigen gene of Tetrahymena thermophila were determined. Primer extension and nuclease protection assays show that the SerH3 transcription unit is 1,425 nucleotides long and contains no introns. The predicted polypeptide encoded by the SerH3 gene has a molecular mass of 44,415 daltons; one-third of its 439 residues are either cysteine, serine, or threonine. The central half of the polypeptide consists of three homologous domains in tandem array; within these domains, the cysteine, proline, and tryptophan residues occur in highly regular patterns.

Amino Acid Sequence↗