scholarly journals Evaluation Of Slovak Winter Wheat Quality In Terms Of Puroindoline Genes

2015 ◽  
Vol 61 (3) ◽  
pp. 88-96 ◽  
Author(s):  
Lenka Klčová ◽  
Daniela Mikulíková ◽  
Štefan Masár ◽  
Alžbeta Žofajová
Keyword(s):  
Winter Wheat ◽  
Null Allele ◽  
Null Alleles ◽  
Width Ratio ◽  
Quality Trait ◽  
Wheat Quality ◽  
Grain Hardness ◽  
Normal Allele ◽  
Wild Type ◽  
Chain Reactions

Abstract The grain hardness of 100 current and 24 old superior Slovak winter wheat cultivars was studied at molecular level. Using polymerase chain reactions (PCRs), normal and null alleles of both puroindoline Pina and Pinb genes were identified. Three different genotypes were found: 1) normal allele of both genes (dominant wild type with soft endosperm) − Pina-D1a/Pinb-D1a; 2) normal allele of the Pina gene and null allele of the Pinb gene – Pina-D1a/Pinb-D1b; and 3) null allele of the Pina gene and normal allele of the Pinb gene Pina-D1b/Pinb-D1a. No Slovak current as well as old wheat cultivar had together null allele of both puroindoline genes. The frequencies of wild-type Pinb-D1a and null Pinb-D1b allele in current cultivars were 62.0% and 38.0%, respectively, whilst in old cultivars, 8.3% and 91.7%, respectively. Regarding null allele Pina-D1b of puroindoline Pina gene, only in Rheia current cultivar, one was found. All other cultivars had wild-type Pina-D1a allele. Alacris, Alana, Axis, Balada, Blava, Bona Dea, Bruta, Charger, Hana, Ilona, IS Karpatia, Ludwig and Sulamit current cultivars were selected as donors of the null Pinb-D1b allele for molecular breeding in order to improve the grain hardness as important wheat quality trait. Statistically significant correlations between null Pinb-D1b allele and grain size as well as colour were found. In comparison with wild type, cultivars with this null allele have paler and longer grain with higher length-to-width ratio and lighter grain colour.

Allotype Reagents Distinguish Donor and Recipient Antibodies after Hematopoietic Transplantation.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2906-2906
Author(s):  
Julie R. Boiko ◽  
Bita Sahaf ◽  
David B. Miklos
Keyword(s):  
Monoclonal Antibodies ◽  
B Cell ◽  
Allele Frequency ◽  
Null Allele ◽  
Competitive Inhibition ◽  
Null Alleles ◽  
Wild Type ◽  
Cell Engraftment ◽  
Human Sera ◽  
Null Allele Frequency

Abstract Allogeneic immune responses provide beneficial graft-versus-leukemia (GVL) and detrimental graft-versus-host disease (GVHD). To characterize allogeneic B cells and their antibodies in relation to GVHD and GVL, antigen specific assays are required to distinguish donor and recipient antibodies. Inherited polymorphisms in heavy chain constant regions of immunoglobulin can be recognized by allotype specific monoclonal antibodies. We hypothesize that B cell reconstitution differs after myeloablative and nonmyeloablative (NMA) HCT with clinical implications. To test this, we developed allotype ELISAs to quantify donor and recipient antibody responses for specific infectious and allogeneic antigens. Human sera were screened by ELISA coating monoclonal antibodies specific for human allotypes (IgG1m(f), m(z), m(a), IgG2m(n), and IgG3m(g1)) at titers providing shared dynamic ranges. Pre-transplant sera from 48 patients and their donors were serially diluted, and allotype-specific immunoglobulin was detected by alkaline phosphatase-conjugated polyclonal anti-human IgG. Allotype-null sera clearly segregated from wild-type sera with 10-fold absorbency differences. Each null phenotype was confirmed by total IgG and isotype-specific quantification. Overall, IgG1m(f) was null in 8 of 96 sera (null allele frequency 29%), and IgG2m(n) was null in 23 of 96 (null allele frequency 48%). Six patients were null for both, and overall 17 of 48 donor/recipient transplant pairs were informative for either allotype. Nulls for the remaining three allotypes were infrequently recognized limiting their clinical utility. Additionally, we measured monoclonal IgG1 purified from 5 multiple myeloma patients identifying three null alleles, one wild-type, and a single intermediate polymorphism. Labeled conjugation of the wild-type monoclonal IgG1 enables competitive inhibition analysis of null allotype improving null allotype sensitivity for engraftment less than 5%. Sera were collected monthly from all HCT patients informative for allotype antibody. Three NMA HCT patients who underwent total lymphoid irradiation and anti-thymoglobulin (TLI/ATG) conditioning have donors that are null for IgG2m(n) and are being prospectively assessed for recipient antibody loss. Their recipient allotype-specific IgG persists at pretransplant recipient levels in all three patients measured six months after NMA HCT, and the lead patient expresses 100% pretransplant recipient allotype antibody ten months after HCT. Conversely, a single NMA patient null for IgG2m(n) with a wild-type donor has no detectable IgG2m(n) donor antibodies four months after HCT despite having 100% donor peripheral B cell engraftment measured 30 days after NMA HCT. In contrast, an informative patient undergoing myeloablative HCT developed 25% IgG2m(n) donor specific antibodies 3 months post-transplant, and 50% at 7 months. Others have reported donor allotype specific antibody achieves full engraftment by 6 months after myeloablative HCT (Van Tol et al. Blood 1996). Our ongoing preliminary studies suggest NMA HCT patients experience delayed donor antibody onset and prolonged recipient antibodies as compared to patients undergoing myeloablative HCT. In order to confirm this, we are measuring antigen-specific donor allotype antibody reconstitution for infectious antigens (EBV and tetanus) and allogeneic H-Y antigens.

scholarly journals IC138 Defines a Subdomain at the Base of the I1 Dynein That Regulates Microtubule Sliding and Flagellar Motility

2009 ◽  
Vol 20 (13) ◽  
pp. 3055-3063 ◽  
Author(s):  
Raqual Bower ◽  
Kristyn VanderWaal ◽  
Eileen O'Toole ◽  
Laura Fox ◽  
Catherine Perrone ◽  
...  
Keyword(s):  
Double Mutant ◽  
Essential Role ◽  
Null Allele ◽  
Flagellar Motility ◽  
Wild Type ◽  
Gene Encoding ◽  
Radial Spoke ◽  
Mutant Strains ◽  
Dynein Arms ◽  
Image Averaging

To understand the mechanisms that regulate the assembly and activity of flagellar dyneins, we focused on the I1 inner arm dynein (dynein f) and a null allele, bop5-2, defective in the gene encoding the IC138 phosphoprotein subunit. I1 dynein assembles in bop5-2 axonemes but lacks at least four subunits: IC138, IC97, LC7b, and flagellar-associated protein (FAP) 120—defining a new I1 subcomplex. Electron microscopy and image averaging revealed a defect at the base of the I1 dynein, in between radial spoke 1 and the outer dynein arms. Microtubule sliding velocities also are reduced. Transformation with wild-type IC138 restores assembly of the IC138 subcomplex and rescues microtubule sliding. These observations suggest that the IC138 subcomplex is required to coordinate I1 motor activity. To further test this hypothesis, we analyzed microtubule sliding in radial spoke and double mutant strains. The results reveal an essential role for the IC138 subcomplex in the regulation of I1 activity by the radial spoke/phosphorylation pathway.

Abstract 12291: Contribution of Rare Mutations in Mendelian Hypercholesterolemia Genes to Risk for Premature Coronary Artery Disease in the Population

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Hong-Hee Won ◽  
Ron Do ◽  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Null Allele ◽  
Coronary Revascularization ◽  
Null Alleles ◽  
Premature Coronary Artery Disease ◽  
Rare Mutations ◽  
Increased Risk ◽  
Artery Disease ◽  
Cad Risk

Introduction: Low-density lipoprotein cholesterol (LDL-C) is a causal risk factor for coronary artery disease (CAD). Rare mutations in at least 6 genes lead to Mendelian forms of high or reduced LDL-C; three ( APOB, LDLR, PCSK9 ) act in a dominant pattern whereas three ( ABCG5, ABCG8, LDLRAP1 ) in a recessive pattern. We address to what extent rare mutations in Mendelian LDL-C genes contribute to early CAD risk in the population. Methods: We sequenced the exons of the 6 genes in 9,329 early CAD cases (myocardial infarction, angiographic CAD, or coronary revascularization in men≤50 and women≤60) and 10,245 controls from 9 studies using targeted and whole exome next-generation sequencing. We tested 3 sets: ‘Null alleles’ (nonsense, splice-site, or frameshift); ‘Deleterious (7/7)’ (null and missense annotated as damaging by 7 algorithms); and ‘Deleterious (6/7)’ (null and missense annotated as damaging by at least 6 algorithms). Given the rarity of deleterious mutations, we aggregated these mutations in each gene and tested for an excess or deficit in cases vs . controls. Results: Counts of mutations are provided in Table. Null mutations in LDLR , carried by 1:500 participants, confered a 8-fold increase in CAD risk (P=8х10 -7 ) whereas heterozygosity for a null mutation in ABCG5 (1:650 frequency) was associated with a 3-fold increased risk (P=5х10 -3 ). ‘Deleterious (7/7)’ mutations in LDLR , carried by 1:100 participants, confered a 4-fold increased risk (P=8х10 -17 ) whereas heterozygosity for a ‘Deleterious (7/7)’ mutation in ABCG5 (1:250 frequency) was associated with a 2-fold increased risk (P=2х10 -3 ). Heterozygous null allele carriers at LDLR and ABCG5 had increased LDL-C (P<0.001). Conclusions: Of early CAD cases, 2-3% carry a rare, deleterious mutation at LDLR or ABCG5 associated with increased risk. Although previously reported to cause recessive sitosterolemia, we find that heterozygosity for a null allele at ABCG5 is associated with markedly higher early CAD risk.

Abstract 495: GSTM1 Deficiency Exacerbates Hypertension in the Remnant Model of Chronic Kidney Disease

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Sylvia Cechova ◽  
Rosa Chan ◽  
Beverly Koller ◽  
Thu H Le
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Null Allele ◽  
Null Alleles ◽  
Hypertensive Nephrosclerosis ◽  
Baseline Systolic Blood Pressure ◽  
Glutathione S Transferases ◽  
Targeting Strategy ◽  
Multiple Chronic Diseases

There is a general consensus that oxidative stress is a factor in the progression of chronic kidney disease (CKD). Hence, genetic variants that affect the capacity to handle oxidative stress may influence the outcomes of CKD. One important class of enzymes that has evolved to combat the damaging effects of reactive oxygen species is the glutathione-S-transferases. In particular, the μ class isoform 1 (GSTM1) has emerged as a potential modifier of multiple chronic diseases in humans. Approximately 30%-50% of humans are completely deficient of the GSTM1 enzyme because of homozygous inheritance of the GSTM1 null allele, GSTM1(0). We have identified the GSTM1 gene as a modifier of disease progression in hypertensive nephrosclerosis (HN). In an ancillary study of the African American (AA) Study of Hypertension and Kidney Disease (AASK) Trial, we reported that participants carrying one ( 1/0 ) or two ( 0/0 ) null alleles had 1.7- and 2-fold higher risk of the composite outcome of a 50% decline in the glomerular filtration rate (GFR), dialysis, or death relative to those with two active alleles. Here, the objective of our study was to determine the consequence of deletion of Gstm1 on the course of chronic kidney disease induced by reduction of renal mass (RRM) model in mice. We generated Gstm1-/- (KO) mice on the 129S6 background through conventional gene targeting strategy. By radiotelemetry, Gstm1 KO mice displayed a modest but significantly higher baseline systolic blood pressure (SBP) compared to their wild type (WT, Gtsm1 +/+ ) littermates: KO (n = 5): 138.8 ± 1.3; WT (n = 5): 132.1 ± 1.1, p < 0.01. Baseline urinary isoprostane (ng/100 mg of body weight) was significantly higher in KO mice than WT mice (15.1 ± 2.9; WT: 8.0 ± 0.8, p < 0.04). Four weeks after sub-total nephrectomy, Gstm1 KO mice developed significantly more severe hypertension than WT mice. The average SBP over a 2 week recording by radiotelemetry was 154.0 ± 3.2 mm Hg in KO mice (n = 5), and 142.3 ± 4.2 in WT mice (n = 3), p < 0.01. The effects of deletion of Gstm1 on kidney function and histopathology are under investigation. In conclusion, loss of GSMT1 increases oxidative stress and exaggerates hypertension in the murine model of chronic kidney disease.

scholarly journals Molecular genetics of cryptopleurine resistance in Saccharomyces cerevisiae: expression of a ribosomal protein gene family.

Genetics ◽  
1993 ◽  
Vol 135 (3) ◽  
pp. 719-730
Author(s):  
A G Paulovich ◽  
J R Thompson ◽  
J C Larkin ◽  
Z Li ◽  
J L Woolford
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Ribosomal Protein ◽  
Gene Fusion ◽  
Null Allele ◽  
Ribosomal Subunit ◽  
Null Alleles ◽  
Protein Synthesis Inhibitor ◽  
Lacz Gene ◽  
Ribosomal Subunits ◽  
Cry1 Gene

Abstract The Saccharomyces cerevisiae CRY1 gene encodes the 40S ribosomal subunit protein rp59 and confers sensitivity to the protein synthesis inhibitor cryptopleurine. A yeast strain containing the cry1-delta 1::URA3 null allele is viable, cryptopleurine sensitive (CryS), and expresses rp59 mRNA, suggesting that there is a second functional CRY gene. The CRY2 gene has been isolated from a yeast genomic library cloned in bacteriophage lambda, using a CRY1 DNA probe. The DNA sequence of the CRY2 gene contains an open reading frame encoding ribosomal protein 59 that differs at five residues from rp59 encoded by the CRY1 gene. The CRY2 gene was mapped to the left arm of chromosome X, centromere-proximal to cdc6 and immediately adjacent to ribosomal protein genes RPS24A and RPL46. Ribosomal protein 59 is an essential protein; upon sporulation of a diploid doubly heterozygous for cry1-delta 2::TRP1 cry2-delta 1::LEU2 null alleles, no spore clones containing both null alleles were recovered. Several results indicate that CRY2 is expressed, but at lower levels than CRY1: (1) Introduction of CRY2 on high copy plasmids into CryR yeast of genotype cry1 CRY2 confers a CryS phenotype. Transformation of these CryR yeast with CRY2 on a low copy CEN plasmid does not confer a CryS phenotype. (2) Haploids containing the cry1-delta 2::TRP1 null allele have a deficit of 40S ribosomal subunits, but cry2-delta 1::LEU2 strains have wild-type amounts of 40S ribosomal subunits. (3) CRY2 mRNA is present at lower levels than CRY1 mRNA. (4) Higher levels of beta-galactosidase are expressed from a CRY1-lacZ gene fusion than from a CRY2-lacZ gene fusion. Mutations that alter or eliminate the last amino acid of rp59 encoded by either CRY1 or CRY2 result in resistance to cryptopleurine. Because CRY2 (and cry2) is expressed at lower levels than CRY1 (and cry1), the CryR phenotype of cry2 mutants is only expressed in strains containing a cry1-delta null allele.

scholarly journals Expression of Functional CD32 Molecules on Human NK Cells Is Determined by an Allelic Polymorphism of the FcγRIIC Gene

Blood ◽  
1998 ◽  
Vol 91 (7) ◽  
pp. 2369-2380 ◽  
Author(s):  
Diana Metes ◽  
Linda K. Ernst ◽  
William H. Chambers ◽  
Andrei Sulica ◽  
Ronald B. Herberman ◽  
...  
Keyword(s):  
Nk Cells ◽  
Null Allele ◽  
Nk Cell ◽  
Full Length ◽  
Null Alleles ◽  
Soluble Form ◽  
Allelic Polymorphism ◽  
Reading Frame ◽  
Normal Individuals ◽  
Alternatively Spliced

Human natural killer (NK) cells were thought to express only FcγRIIIA (CD16), but recent reports have indicated that NK cells also express a second type of FcγR, ie, FcγRII (CD32). We have isolated, cloned, and sequenced full-length cDNAs of FcγRII from NK cells derived from several normal individuals that may represent four different products of the FcγRIIC gene. One transcript (IIc1) is identical with the already described FcγRIIc form. The other three (IIc2-IIc4) appear to represent unique, alternatively spliced products of the same gene, and include a possible soluble form. Analyses of the full-length clones have revealed an allelic polymorphism in the first extracellular exon, resulting in either a functional open reading frame isoform or a null allele. Stable transfection experiments enabled us to determine a unique binding pattern of anti-CD32 monoclonal antibodies to FcγRIIc. Further analyses of NK-cell preparations revealed heterogeneity in CD32 expression, ranging from donors lacking CD32 expression to donors expressing high levels of CD32 that were capable of triggering cytotoxicity. Differences in expression were correlated with the presence or absence of null alleles. These data show that certain individuals express high levels of functional FcγRIIc isoforms on their NK cells.

scholarly journals The calculation of recombination frequencies in crosses of allogamous plant species with applications to linkage mapping

1996 ◽  
Vol 67 (1) ◽  
pp. 55-65 ◽  
Author(s):  
E. Ritter ◽  
F. Salamini
Keyword(s):  
Linkage Mapping ◽  
Null Allele ◽  
Null Alleles ◽  
Marker Allele ◽  
Information Functions ◽  
Original Proposal ◽  
Point Estimates ◽  
Allelic Configuration ◽  
Single Marker ◽  
Marker Class

SummaryThe recombination frequency (r) between two loci defined by conventional or molecular markers can be estimated by solving proper Maximum Likelihood equations. These are based on expected and observed marker class frequencies in the progeny of a cross, and are specific for each allelic configuration of the parents(1). In a cross between two diploid parents up to four different alleles, besides a null allele, can be detected at one locus. This defines in each parent, considering a locus A, nine basic allelic configurations based on two allelic marker fragments(Ai/Aj), one single marker allele and a null allele (Ai/AO), or just null alleles (AO/AO). With respect to two loci the consideration of all possible diploid allelic configurations in the parents of a cross allows the detection of 21 different expected marker class distributions producing estimates of r in the progeny. General formulas for calculating the ML equations and the corresponding information functions have been developed for the 21 marker class distributions. Simplified formulas have been also derived and the relative efficiency of the information functions compared. As expected, in the majority of cases, allelic marker configurations give more precise estimates of linkage values than single marker configurations. A method for the construction of linkage maps based on two point estimates, linkage subgroups and allelic bridges is presented. The method is an improvementon an original proposal by Ritter et al.(1990).

scholarly journals Identification of New Flagellar Genes of Salmonella enterica Serovar Typhimurium

2006 ◽  
Vol 188 (6) ◽  
pp. 2233-2243 ◽  
Author(s):  
Jonathan Frye ◽  
Joyce E. Karlinsey ◽  
Heather R. Felise ◽  
Bruz Marzolf ◽  
Naeem Dowidar ◽  
...  
Keyword(s):  
Salmonella Enterica Serovar Typhimurium ◽  
Transcriptional Start Site ◽  
Null Alleles ◽  
Wild Type ◽  
Gene Encoding ◽  
Isolation And Characterization ◽  
Serovar Typhimurium ◽  
Chemotaxis Proteins ◽  
Flagellar Genes ◽  
Rna Levels

ABSTRACT RNA levels of flagellar genes in eight different genetic backgrounds were compared to that of the wild type by DNA microarray analysis. Cluster analysis identified new, potential flagellar genes, three putative methyl-accepting chemotaxis proteins, STM3138 (McpA), STM3152 (McpB), and STM3216(McpC), and a CheV homolog, STM2314, in Salmonella, that are not found in Escherichia coli. Isolation and characterization of Mud-lac insertions in cheV, mcpB, mcpC, and the previously uncharacterized aer locus of S. enterica serovar Typhimurium revealed them to be controlled by σ28-dependent flagellar class 3 promoters. In addition, the srfABC operon previously isolated as an SsrB-regulated operon clustered with the flagellar class 2 operon and was determined to be under FlhDC control. The previously unclassified fliB gene, encoding flagellin methylase, clustered as a class 2 gene, which was verified using reporter fusions, and the fliB transcriptional start site was identified by primer extension analysis. RNA levels of all flagellar genes were elevated in flgM or fliT null strains. RNA levels of class 3 flagellar genes were elevated in a fliS null strain, while deletion of the fliY, fliZ, or flk gene did not affect flagellar RNA levels relative to those of the wild type. The cafA (RNase G) and yhjH genes clustered with flagellar class 3 transcribed genes. Null alleles in cheV, mcpA, mcpB, mcpC, and srfB did not affect motility, while deletion of yhjH did result in reduced motility compared to that of the wild type.

Genetic analysis of small nuclear RNAs in Saccharomyces cerevisiae: viable sextuple mutant

1988 ◽  
Vol 8 (8) ◽  
pp. 3150-3159
Author(s):  
R Parker ◽  
T Simmons ◽  
E O Shuster ◽  
P G Siliciano ◽  
C Guthrie
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Transcriptional Start Site ◽  
Single Copy ◽  
Gene Replacement ◽  
Null Alleles ◽  
Wild Type ◽  
Small Nuclear Rnas ◽  
Apparent Correlation ◽  
Genes Encoding ◽  
Sm Antigen

Saccharomyces cerevisiae contains at least 24 distinct small nuclear RNAs (snRNAs), several of which are known to be essential for viability and to participate in the splicing of pre-mRNAs; the RNAs in this subset contain binding sites for the Sm antigen, a hallmark of metazoan snRNAs involved in mRNA processing. In contrast, we showed previously that the single-copy genes for three other snRNAs (snR3, snR4, and snR10) are not required for viability, although cells lacking snR10 are growth impaired at low temperature. None of these RNAs associates with the Sm antigen. To assess this apparent correlation, we cloned and sequenced the genes encoding three additional non-Sm snRNAs. Comparison of these genes with nine additional yeast snRNA genes revealed a highly conserved TATA box located 92 +/- 8 nucleotides 5' of the transcriptional start site. By using the technique of gene replacement with null alleles, each of these three single copy genes was shown to be completely dispensable. We constructed multiple mutants to test the hypothesis that, individually, each of these snRNAs is nonessential because the snRNAs play functionally overlapping roles. A mutant lacking five snRNAs (snR3, snR4, snR5, snR8, snR9) was indistinguishable from the wild type, and growth of the sextuple mutant was no more impaired than that in strains lacking only snR10. This widespread dispensability of snRNAs was completely unexpected and forces us to reconsider the possible roles of these ubiquitous RNAs.

Differential effectiveness of yeast cytochrome c oxidase subunit genes results from differences in expression not function

1987 ◽  
Vol 7 (10) ◽  
pp. 3520-3526
Author(s):  
C E Trueblood ◽  
R O Poyton
Keyword(s):  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Fusion Gene ◽  
Single Copy ◽  
Chimeric Gene ◽  
Lacz Fusion ◽  
Null Alleles ◽  
Activity Levels ◽  
Wild Type ◽  
Oxidase Subunit

In Saccharomyces cerevisiae, COX5a and COX5b encode two distinct forms of cytochrome c oxidase subunit V, Va and Vb, respectively. To determine the relative contribution of COX5a and COX5b to cytochrome c oxidase function, we have disrupted each gene. Cytochrome c oxidase activity levels and respiration rates of strains carrying null alleles of COX5a or COX5b or both indicate that some form of subunit V is required for cytochrome c oxidase function and that COX5a is much more effective than COX5b in providing this function. Wild-type respiration is supported by a single copy of either COX5a or COX5ab (a constructed chimeric gene sharing 5' sequences with COX5a). In contrast, multiple copies of COX5b or COX5ba (a chimeric gene with 5' sequences from COX5b) are required to support wild-type respiration. These results suggest that the decreased effectiveness of COX5b is due to inefficiency in gene expression rather than to any deficiency in the gene product, Vb. This conclusion is supported by two observations: (i) a COX5a-lacZ fusion gene produces more beta-galactosidase than a COX5b-lacZ fusion gene, and (ii) the COX5a transcript is significantly more abundant than the COX5b transcript or the COXsba transcript. We conclude that COX5a is expressed more efficiently than COX5b and that, although mature subunits Va and Vb are only 67% homologous, they do not differ significantly in their ability to assemble and function as subunits of the holoenzyme.

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