A third class I major histocompatibility complex antigen encoded by a gene in the D region of the H-2 d haplotype recognized by cytotoxic T lymphocytes

The D region of the H-2 ^d haplotype contains five class I genes: H-2D ^d , D2 ^d , D3 ^d , D4 ^d and H-2L ^d . Although previous studies have suggested the presence of D-end encoded class I molecules in addition to H-2D^d and H-2L^d, segregation of genes encoding such molecules has not been demonstrated. In this report we have used cãtotoxic T lymphocytes (CTL) to examine the D region of the H-2 ^d haplotype for the presence of additional class I molecules. CTL generated in (C3H × B6.K1)F₁ (K ^k D ^k , K ^b D ^b ) mice against the hybrid class I gene product Q10^d/L^d expressed on L cells cross-react with H-2L^d but not H-2D^d molecules, as determined by lysis of transfected cells expressing H-2L^d but not H-2D^d. Although H-2L^d-specific monoclonal antibodies (mAb) completely inhibit H-2L^d-specific CTL from killing B10.A(3R) (K ^b D ^d L ^d ) target cells, only partial inhibition of anti-Q10 CTL-mediated lysis was observed, suggesting the presence of an additional D-end molecule as a target for these latter CTL. To identify the region containing the gene encoding the Q10 cross-reactive molecule, we show that anti-Q10 CTL lyse target cells from a D-region recombinant strain B10.RQDB, which has H-2D ^d , D2 ^d , D3 ^d , D4 ^d , and H-2D ^b but not the H-2L ^d H-2 ^d , and H-2L ^d (including D2 ^d , D3 ^d , and D4 ^d , lacks this anti-Q10 CTL target molecule. Together, these data demonstrate that a class I gene mapping between H-2D ^d and H-2L ^d encodes an antigen recognozed by anti-Q10 CTL. A likely candidate for this gene is D2 ^d , D3 ^d or D4 ^d .     

The female-killing chromosome of the silkworm, Bombyx mori, was generated by translocation between the Z and W chromosomes

Bombyx mori is a female-heterogametic organism (female, ZW; male, ZZ) that appears to have a putative feminizing gene (Fem) on the W chromosome. The paternally transmitted mutant W chromosome, Df(p ^Sa + ^p W + ^od )Fem, derived from the translocation-carrying W chromosome (p ^Sa + ^p W + ^od ), is inert as femaleness determinant. Moreover, this Df(p ^Sa + ^p W + ^od )Fem chromosome has been thought to have a female-killing factor because no female larvae having the Df(p ^Sa + ^p W + ^od )Fem chromosome are produced. Initially, to investigate whether the Df(p ^Sa + ^p W + ^od )Fem chromosome contains any region of the W chromosome or not, we analyzed the presence or absence of 12 W-specific RAPD markers. The Df(p ^Sa + ^p W + ^od )Fem chromosome contained 3 of 12 W-specific RAPD markers. These results strongly indicate that the Df(p ^Sa + ^p W + ^od )Fem chromosome contains the region of the W chromosome. Moreover, by using phenotypic and molecular markers, we confirmed that the Df(p ^Sa + ^p W + ^od )Fem chromosome is connected with a partially deleted Z chromosome and that this fused chromosome behaves as a Z chromosome during male meiosis. Furthermore, we demonstrated that the ZZW-type triploid female having the Df(p ^Sa + ^p W + ^od )Fem chromosome is viable. Therefore, we concluded that the Df(p ^Sa + ^p W + ^od )Fem chromosome does not have a female-killing factor but that partial deletion of the Z chromosome causes the death of the ZW-type diploid female having the Df(p ^Sa + ^p W + ^od )Fem chromosome. Additionally, our results of detailed genetic analyses strongly indicate that the female-killing chromosome composed of the Df(p ^Sa + ^p W + ^od )Fem chromosome and deleted Z chromosome was generated by translocation between the Z chromosome and the translocation-carrying W chromosome, p ^Sa + ^p W + ^od .     

Cross-reactivity between RSV-induced tumor antigen and B5 MHC alloantigen in the chicken

Lymphocytes from chickens homozygous (B ² B ²) at the major histocompatibility complex (MHC) were tested for cytotoxic activity against five types of target chicken embryo fibroblasts (CEF). Lymphocytes from B²B² chickens bearing RSV-induced tumors lysed in vitro targets of B ² B ² and B ⁵ B ⁵ RSV-infected CEF and B ⁵ B ⁵ normal CEF, but did not lyse B ² B ² and B ²⁴ B ²⁴ normal CEF. Lymphocytes from normal B ² B ² chickens did not lyse any of the five types of CEF targets. Alloantisera absorption studies showed that both RSV-infected and uninfected CEF shared alloantigens, in particular B-F alloantigens, with syngeneic erythrocytes. Absorption with B ² B ² RSV-infected CEF significantly lowered the titer of B ² B ² anti-B ⁵ B ⁵ alloantisera. Cross-reactivity between B ₅ antigen(s) and tumor-associated antigen was suggested and the nature of the cross-reactivity was discussed. It is hypothesized that this cross-reactivity prevents B ⁵ B ⁵ chickens from recognizing RSV-induced tumors as foreign, enhances tumor growth and leads to death of the host.     

Mapping of susceptibility to Marek's disease within the major histocompatibility (B) complex by refined typing of White Leghorn chickens

The major histocompatibility (B) complex of a distinct commercial pure White Leghorn chicken line was characterized using serological, biochemical and restriction fragment length polymorphism (RFLP) typing. Line B chickens displayed a high recombination frequency within the B complex. Three recombinant haplo-types were identified. The influence of these haplotypes was determined in relation to the haplotypes B^l9 and B²¹ on their resistance to Marek's disease (MD) in an experimental infection with the virus. Offspring of sires with a recombinant haplotype in combination with B¹⁹ or B²¹, and dams, which were homozygous B¹⁹/B¹⁹ or B²¹/B²¹ were infected. The B type of the offspring had a significant effect upon survival. Animals with B complex types B²¹/B²¹, B¹³⁴/B²¹ and B²³⁴/B²¹ were relatively resistant to MD (24–32% mortality), whereas B¹⁹/B¹⁹ birds were highly susceptible (68% mortality). Animals with a recombinant halpotype B^19r21 (B-G²¹, B-F¹⁹) were equally susceptible to MD as birds with the complete B¹⁹ haplotype. In contrast to earlier publications, resistance was not inherited as a dominant trait. Apparently, B¹⁹ was associated with a dominant susceptibility. The gene(s) associated with the B complex and involved in resistance to MD were localized within the B-F/B-L region. However, the association with a presumably non-coding subregion of B-G could not be excluded.     

Detection of three virulence genes alt, ahp and aerA in Aeromonas hydrophila and their relationship with actual virulence to zebrafish

Aims: To evaluate the frequency of the aerolysin (aerA), cytotoxic enterotoxin (alt) and serine protease (ahp) genes in Aeromonas hydrophila isolates from different sources, and to determine the relationship between the presence of these genes and virulence of A. hydrophila in zebrafish. Methods and Results: Aeromonas hydrophila isolates from clinical cases (n = 40), from healthy fish (n = 22) and from water environment (n = 21) were analysed with respect to the prevalence of aerA, alt and ahp genes by PCR assay. These virulence factors occur among clinical isolates as well as among isolates from healthy fish and water environment. The majority (97·6%) of the strains examined carried one or more virulence genes. The isolates were divided into seven genetic profiles on the basis of PCR result: aerA⁺alt⁺ahp⁺ (62·7%), aerA⁺alt⁺ahp^? (13·3%), aerA⁺alt^?ahp⁺ (10·8%), aerA^?alt⁺ahp⁺ (4·8%), aerA^?alt^?ahp⁺ (3·6%), aerA⁺alt^?ahp^? (2·4%) and aerA^?alt^?ahp^? (2·4%). A higher frequency of genetic group aerA⁺alt⁺ahp⁺ was determined in the isolates from diseased animals compared to those from healthy fish or water environments. Virulence properties of 26 representative strains belonging to the seven genetic profiles were further characterized. Results demonstrated that as the present of virulence genes increased, the proteolytic, haemolytic and cytotoxic activities of extracellular products also increased. And the 50% lethal doses (LD₅₀s) of aerA⁺alt⁺ahp⁺ isolates (<10⁵) in zebrafish were lower when compared with the strains expressing one or combinations of two virulence genes (>10⁶). Conclusions: Virulence properties of A. hydrophila correlated well with the presence of virulence genes tested. aerA⁺alt⁺ahp⁺ was more frequent virulence genotype in A. hydrophila isolates from clinical diseases than from healthy fish and water environment, and the aerA⁺alt⁺ahp⁺ isolates were more virulent to zebrafish compared to the other six genetic profiles. Significant and Impact of the Study: The detection for aerA, alt and ahp can be used for virulence typing of A. hydrophila isolates.     

Influence of different B-complex recombinants on the outcome of Rous sarcomas in chickens

Seven major histocompatibility (B) complex recombinants were evaluated for anti-Rous sarcoma response. In experiment 1, the B^R5(F21-G19) recombinant haplotype both homozygous and in heterozygous combinations with B¹⁹ and B²¹ haplotypes were compared to B¹⁹/B¹⁹ and B²¹/B²¹ chickens to determine the relative influence of the B^F versus B^G chromosomal segments on regression of Rous sarcoma virus-induced tumours. In experiment 2, six recombinant haplotypes B^R1(F24-G23), B^R2(F2-G23), B^R3(F2-G23), B^R4(F2-G23), B^R6(F21-G23) and B^R8(F2-G2a,23) present in chickens heterozygous for normal haplotypes B¹⁹, B²³ or B²⁶ were compared for anti-sarcoma response. A total of 1328 chickens were blood typed for B alloanti-gens at 17 days of age, inoculated in the wingweb with Rous sarcoma virus at 6 weeks and monitored for anti-tumour immune response over a 10-week period. Genotypes which shared the same B^F haplotype, but differed in their B^G regions, had similar anti-tumour responses, implicating the B^F but not the B^G region in tumour regression. Chickens carrying B^F2 or B^F21 had a strong anti-tumour response, while B^F24 conferred a weaker response, regardless of the accompanying normal haplotype.     

Immune responses in vitro

The Mls locus was originally defined to have four alleles; three controlled products that were detectable in primary mixed leukocyte reactions (MLR), whereas one, b, was described as being null. Recently, other investigators postulated that the Mls locus is nonpolymorphic, being composed of the b null allele and of a singly expressed allele previously thought to be the a and d alleles. We previously reported that products controlled by Mls ^aand Mls ^dwere antigenically distinct and therefore are not controlled by the same allele, and the product of Mls ^bon cells of three different strains was easily detectable by Mls ^aand Mls ^dresponding cells. Thus the b allele is not null. In the present report evidence is presented which indicates that both Mls ^band Mls ^cencoded products were undetectable by MLR when in the presence of Mls ^aor Mls ^d. This was demonstrated by (a) the inability of Mls ^a/Mls ^cand Mls ^a/Mls ^bF₁ cells to stimulate Mls ^aresponding cells and Mls ^d/Mls ^cand Mls ^d/Mls ^bcells to stimulate Mls ^dcells; (b) the positive response of Mls ^a/Mls ^band Mls ^d/Mls ^bF₁-hybrid cells to Mls ^b-encoded products; and (c) the reactivity of Mls ^a/Mls ^cand Mls ^d/Mls ^cF₁ hybrid cells to Mls ^c-encoded determinants.     

Intra-H-2 recombination in the mouse

Serological characterization of threeK-S interval recombinant strains, TBR2 (H-2 ^at2 ), TBR3 (H-2 ^at3 ) and AIR1 (H-2 ^a2 ) was performed using anti-H-2, Ia, Ss and Slp antisera. The data presented here reveal that the crossover events in both TBR2 and TBR3 occurred between theI-A andI-E subregions. In both cases, theH-2K andI-A subregions were derived from theH-2 ^t1 chromosome, while theI-E, S andH-2D regions were derived from theH-2 ^b chromosome (K ^s A ^k E ^b S ^b D ^b ). TheH-2 ^a2 chromosome resulted from a crossover event between theH-2 ^a1 andH-2 ⁱ⁹ chromosomes. Ia and Ss typing of AIR1 suggested that theK toI-E regions originated fromH-2 ^a1 and theS andD regions originated fromH-2 ⁱ⁹ (K ^k A ^k E ^k S ^b D ^d ).     

Do histocompatibility antigens recognize themselves?

In the Simonsen spleen weight assay, theH-2K ^ba mutant does not respond against theH-2K ^bd mutant orH-2K ^bd /H-2K ^b hybrid, while the parentalH-2K ^b haplotype does respond. TheH-2K ^ba /H-2K ^b hybrid reacts strongly to bothH-2K ^bd andH-2K ^bd /H-2K ^b , indicating that the donor genotype could influence the reactivity against the same antigenic difference. The response of theH-2 ^ba mutant against a number of unrelated H-2 antigens does not differ from that of the parental haplotype. TheH-2K ^bd mutant reacts againstH-2K ^b andH-2K ^ba , and theH-2K ^b parent reacts against both theH-2K ^ba andH-2K ^bd mutants. The specific defect of reactivity in theH-2K ^ba mutant is effectively complemented by crossing with a number of unrelatedH-2 haplotypes. TheH-2 ^ka andH-2 ^fa mutants complement poorly compared to corresponding parental strains CBA and A.CA, while the B10.M (H-2 ^f ) strain does not complement at all (which is probably attributable to an undetectedH-2 mutation in the last strain). The data strongly suggest that the product of theH-2K locus-which is known to function as a transplantation antigen, lymphocyte activating determinant, and serologically defined antigen-also influences the immune response capacity against a mutant histocompatibility determinant.     

Distribution of hereditary blood groups among Indians in South America. I. In Ecuador

Blood specimens were procured from 658 Quechua, 36 Colorado, 233 Jivaro, 244 Cayapa, and 48 Secoya Indians of Ecuador. These were examined for antigens in the A-B-O, M-N-S-s, P, Rh-Hr, Lutheran, K-k, Lewis, Duffy and Kidd systems and for Diego (Di^a), Wright (Wr^a), and Berrens (Be^a) agglutinogens as well. Hemolystes were prepared and studied for hemoglobin types and the serum samples were tested for haptoglobins and transfserrins. Gene frequencies are high for O, M, s, R¹, (CDe), R² (cDE), Lu^b, k, Kp^b, Le^b and Fy^a; and low or absent for A, B, N, S, Mi^a, Vw, Mt^a, R⁰ (cDe), V (ce^s), Lu^a, K, Kp^a, Le^a, Fy^b, Js^a, Wr^a and Be^a. The Diego (Di^a) gene is present but its frequency varies greatly from tribe to tribe. Gene frequency Hp¹ is well within the range previously reported for Indians in Middle America excepting the Colorado in which population the frequency of 0.889 is unusually high. All 723 serum specimens tested for transferrins were C or CD. No D or BC types were found. All Ecuadorian Indian bloods tested electrophoretically contained only hemoglobin (A) as a major component.     

Extrachromosomal inheritance inSchizosaccharomyces pombe

Summary Spontaneous chloramphenicol (cap ^r)- and erythromycin (ery ^r)-resistant mutants were isolated from strain ade7–50 h ^- and the antimycin-resistant mutant ana ^r-8 ade 7–50 h^- of Schizosaccharomyces pombe (Sch. p.). By mitotic segregation analysis all 154 cap ^r- and 120 ery ^r-mutants derived from ade 7–50 h ^- proved to be recessive chromosomal, whereas all 108 cap ^r- and 200 ery ^r-mutants originating from ana ^r-8 were extrachromosomally inherited. The rate of spontaneous cap ^r- and ery ^r-mutants was about hundredfold in ana ^r-8 compared to ade 7–50 h ^-. Growth of cap ^r-and ery ^r-mutants was not inhibited by chloramphenicol or erythromycin, respectively, in glucose-medium and only slightly in glycerol-medium at concentrations which completely inhibited ana ^r-8. By mitotic segregation-, tetrad-, and mitotic haploidization-analysis the extrachromosomal inheritance of mutants derived from ana ^r-8 was established. Segregational patterns of cap ^r- and ery ^r-determinats during mitosis, meiosis, and mitotic haplidization of diploids are discussed.     

A new ENU-induced allele of mouse quaking causes severe CNS dysmyelination

The mutant allelic series of the mouse quaking gene consists of the spontaneous quaking^viable (qk^v) allele, which is homozygous viable with a dysmyelination phenotype, and four ENU-induced alleles (qk^kt1, qk^k2, qk^kt3/4, and qk^l-1), which are homozygous embryonic lethal. Here we report the isolation of qk^e5, the first ENU-induced viable allele of quaking. Unlike qk^v/qk^v, qk^e5/qk^e5 animals have early-onset seizures, severe ataxia, and a dramatically reduced lifespan. Ultrastructural analysis of qk^e5/qk^e5 brains reveals severe dysmyelination when compared with both wild-type and qk^v/qk^v brains. In addition, Calbindin detection in young adult qk^e5/qk^e5 mice reveals Purkinje cell axonal swellings indicative of neurodegeneration , which is not seen in young adult qk^v/qk^v mice. Although the molecular defect in the qk^e5 allele is not evident by sequencing, protein expression studies show that qk^e5/qk^e5 postnatal oligodendrocytes lack the QKI-6 and QKI-7 isoforms and have reduced QKI-5 levels. The oligodendrocyte developmental markers PDGFαR, NG2, O4, CNP, and MBP are also present in the qk^e5/qk^e5 postnatal brain although CNP and MBP levels are considerably reduced. Because the qk^v allele is a large deletion that affects the expression of three genes, the new neurologic qk^e5 allele is an important addition to this allelic series.     

Molecular structure of rare but geographically widespread sn-glycerol-3-phosphate dehydrogenase ‘ultra-fast’ electrophoretic alleles in Drosophila melanogaster

Six naturally occurring but rare alleles of sn-glycerol-3-phosphate dehydrogenase (Gpdh) in Drosophila melanogaster have been investigated in this study. They all belong to a class of Gpdh ^UF (ultra-fast) alleles, because their electrophoretic mobilities are faster than that of the Gpdh ^F (fast) allele. The Gpdh ^UF variants are widespread, and have been reported from five continents. DNA sequence analysis has shown that the change in electrophoretic mobility was in each allele caused by a single amino acid residue substitution in the encoded protein. In the Xiamen ^UF allele it is a substitution of lysine (AAA) to asparagine (AAT) in exon 1 (residue 3). An asparagine (AAT) to aspartate (GAT) change was found in exon 6 (residue 336) in the Iowa ^UF and Netherlands ^UF alleles. The mobility of the Raleigh ^UF allele was altered by a valine (GTG) to glutamate (GAG) substitution in exon 3 (residue 76). Two mutations were detected in the Brazzaville ^UF allele: a lysine (AAG) to methionine (ATG) substitution in exon 2 (residue 68) is responsible for the ultra-fast phenotype of this variant, while a tyrosine (TAT) to phenylalanine (TTT) substitution in exon 4 (residue 244) is not expected to alter the electrophoretic mobility of the encoded protein. These results indicate that the Gpdh ^UF alleles originate from different mutational events, and only two of them — Iowa ^UF and Netherlands ^UF — might share a common ancestry. The GPDH activity of the Iowa ^UF allele is intermediate between those of the Gpdh ^S and Gpdh ^F control stocks. The other Gpdh ^UF variants have lower activities than the controls: Xiamen ^UF -83%, Raleigh ^UF -80% and Brazzaville ^UF -73% of the Gpdh ^F control.     

Effects of light-dark cycles on the circadian conidiation rhythm inNeurospora crassa

The effects of 24 hr light-dark cycles on the circadian conidiation rhythm inNeurospora crassa were compared among will-typefrq ⁺ and clock mutantsfrq ⁺,frq ³,frq ⁷,frq ⁹ andfrq ¹¹. The minimum length of the light period necessary for complete entrainment to the light-dark cycles was almost 2 hr infrq ⁺,frq ³ andfrq ⁷ strains. The minimum duration of the dark period necessary for the appearance of circadian conidiation was almost 4 hr in all of the strains except thefrq ¹¹ strain. The phase of the conidiation rhythm was dependent on the light to dark transition in thefrq ¹ strain in all light-dark cycles examined and in thefrq ⁺ andfrq ³ strains when the light period was shorter than 16 hr. In contrast, the phase of thefrq ⁷ strain was dependent on the light to dark transition when the light period was shorter than 10 hr.     

Genetic variability in the European minnow,Phoxinus phoxinus (L.)

An electrophoretic study of genetic variation at 11 loci was performedfor a population of European minnows, Phoxinus phoxinus (L.). Ten loci, EST-1 ^*, EST-2 ^* EST-3 ^*,GPD-1 ^*,GPD-2 ^*,GPI-1 ^*,GPI-2 ^*,MPI ^*,6PGD ^* and PGM ^* were polymorphic. IDH ^*wasmonomorphic. The mean number of heterozygotic loci over all 176 fish was 3.05 ± 0.104(SE). Observed mean heterozygosity was 0.28±0.058(SE) and expected mean heterozygosity was 0.27±0.054(SE). EST-2 ^*, EST-3 ^* andPGM ^* were not in Hardy-Weinberg equilibrium. Length,condition, parasite numbers or male breeding characters, i.e. red colorationand tubercles, were not influenced by single enzyme loci.     

HYBRIDOGENESIS AND ANDROGENESIS IN THE STICK-INSECT BACILLUS ROSSIUS-GRANDII BENAZZII (INSECTA,PHASMATODEA)

In northwestern Sicily interspecific hybrid females between Bacillus rossius and B. grandii benazzii (Insecta, Phasmatodea) are sympatric with facultatively parthenogenetic demes of the former and bisexual populations of the latter. Preliminary observations suggested that hybrid females are maintained by hybridogenetic reproduction, not by current F₁ hybrid production nor through parthenogenesis. Being hybridogens, a complex of hemiclonal lineages, we informally refer to them as B. rossius-grandii benazzii, according to Schultz's proposal. In this study B. rossius-g. benazzii females were crossed with males of B. g. benazzii, B. g. grandii, B. g. maretimi, and B. rossius. Allozyme analysis of the progeny showed that the great majority of them were actually produced by hybridogenesis with a hemiclonal inheritance of the maternal B. rossius genotype (Br^m) and actual syngamy with a sperm from the fathering male, so that Br^m-gb^p, Br^m-gg^p, Br^m-gm^p, and Br^m-r^p offspring were obtained in the respective crosses. All-paternal progeny (androgenetics) were also produced (Bgb^pgb^p, Bgm^pgm^p, Br^pr^p) and two gynogenetic descendants were observed. Cytological investigations on virgin eggs that failed to hatch revealed in most of them a haploid-diploid blocked blastoderm; this rudimentary parthenogenesis appears to be an important prerequisite for further evolution of this hybridogen. Reproductive modes of descendants were also analyzed; although Br^m-g^p hybrids are still able to reproduce by hybridogenesis, a progressive disruption of the hybridogenetic-androgenetic system takes place in synthetic B. rossius (Br^m-r^p, Br^pr^p) and abundant thelytokous parthenogenetic offspring are obtained from females of androgenetic origin. The evolutionary role of these hybridogens appears to be linked to their shift towards parthenogenesis; this has apparently occurred in the southeastern Sicilian hybrid B. whitei (=B. rossius/g. grandii), which exhibits both hybridogenesis and parthenogenesis.     

Analysis of merodiploids of the cysB region in Salmonella typhimurium.

Summary We have studied the regulation of two cysteine biosynthetic enzymes in S. typhimurium merodiploid strains which are heterozygous at the cysB regulatory locus. This gene codes for an element of positive control which is necessary for the expression of the enzymes of the biosynthetic pathway. Under conditions of sulfur deprivation levels of sulfite reductase (coded for by cysI, cysJ and cysG) and of O-acetylserine sulfhydrylase (coded for by cysK) are derepressed in cysB ⁺ haploid strains, but not in cysB ^- haploid strains. Growth on a rich sulfur source such as l-cystine results in low levels of both enzyme activities in cysB ⁺ and cysB ^- haploid strains but not in cysB ^c haploid strains, where enzyme expression is constitutive, i.e. substantially greater than in a cysB ⁺ strain grown on l-cystine, regardless of the nutrients used for growth.We find that cysB ^-/F cysB ⁺ merodiploid strains can be derepressed for sulfite reductase and O-acetylserine sulfhydrylase by growth on a poor sulfur source, and therefore cysB ⁺ is dominant to cysB ^-. Enzyme levels are also derepressed in l-cystine-grown cysB ^c/F cysB ⁺ strains indicating that cysB ^c is dominant to cysB ⁺. The cysB484 allele is known to be cysB ^- in regard to the regulation of sulfite reductase activity, but cysB ^c with respect to O-acetylserine sulfhydrylase. In a cysB484/F cysB ⁺ strain the cysB ^- character of cysB484 is recessive to cysB ⁺, while cysB ^c is dominant to cysB ⁺.Merodiploids of the type cysB ^-/F cysB ⁺, bearing chromosomal point mutations are derepressed by sulfur deprivation to levels which are either less than, equal to, or greater than those of wild type. These results can be explained by assuming a multimeric structure for the cysB protein and the formation in merodiploids of cysB ^-/cysB ⁺ hybrid molecules with altered capacities for gene activation. The dominance of cysB ^c over cysB ⁺ indicates that in contrast to the araC regulatory protein, which acts as both a gene activator and repressor, the cysB protein serves only as an element of positive control.     

Hybrid (combinatorial) Ia specificities: Gene complementations to generate Ia.22

Ia specificity 22 is expressed on a hybrid I-E molecule formed by the association of a beta chain (Ae) coded for by the I-A subregion and an alpha chain (E) encoded by the I-E subregion. Ia.22 can be generated by the complementation of A ^b , A ^k A ^s , A ^r with E ^d , E ^k , E ^vp , E ^r , E ^w3 , E ^u , E ^v but not E ^b , E ^f , E ^q , and E ^s . With the exception of H-2 ^p which does not complement with A ^s to generate Ia.22, all Ia.7-positive (I-E) haplotypes can provide the permissive E allele. It is postulated that Ia.22 is a combinatorial Ia determinant generated by the association of the alpha and beta chains. These determinants are probably involved in the immune recognition of antigens under dual Ir-gene control.