Chromosomal localization of two human zinc finger protein genes, ZNF24 (KOX17) and ZNF29 (KOX26), to 18q12 and 17p13-p12, respectively

Two members of the zinc finger Krüppel family, ZNF24 (KOX17) and ZNF29 (KOX26), have been localized by somatic cell hybrid analysis and in situ chromosomal hybridization to human chromosomes 18q12 and 17p13-p12, respectively. The mapping of ZNF29 together with the previously reported localization of ZFP3 suggests that a zinc finger gene complex is located on human chromosome 17p. ZNF29 maps centromeric to the human p53 tumor antigen gene (TP53). In the analogous murine position, the two mouse zinc finger genes Zfp2 and Zfp3 have recently been assigned to the distal region of mouse chromosome 11, the murine homolog of human chromosome 17. Both human zinc finger genes ZNF24 and ZNF29 are in chromosomal regions that have been noted to be deleted in neoplasms of the lung and of the central nervous system at chromosome 17p and in colorectal neoplasia at chromosomes 17p and 18q.     

Chromosomal localization of 9 KOX zinc finger genes: physical linkages suggest clustering of KOX genes on chromosomes 12, 16, and 19

Nine KOX zinc finger genes were localized on four human chromosomes by in situ hybridization of cDNA probes to metaphase chromosomes. KOX1 (ZNF10), KOX11 (ZNF18), and KOX12 (ZNF19) were mapped to chromosome bands 12q24.33, 17p13-p12, and 16q22-q23, respectively. Six other KOX genes were localized on chromosome 19: KOX6 (ZNF14) and KOX13 (ZNF20) to 19p13.3-p13.2, KOX5 (ZNF13) and KOX22 (ZNF27) to 19q13.2-qter, and KOX24 (ZNF28) and KOX28 (ZNF30) to 19q13.4. Pulsed field gel electrophoresis experiments showed that the pairs of KOX genes found on the chromosome bands 12q24.33, 16q22-q23, 19p13.3-p13.2, or 19q13.3-qter lie within 200–300 kb DNA fragments. This suggests the existence of KOX gene clusters on these chromosomal bands.     

Assignment to chromosome 12q24.33, gene organization and splicing of the human KRAB/FPB containing zinc finger gene ZNF84

FISH analysis was used to assign the human ZNF84 gene to chromosome 12q24.33, a region associated with recurrent breakpoints and allelic loss in several human cancers. In this report we show that the ZNF84 coding region is organized in four exons; two are dedicated to encoding the KRAB/FPB-A and KRAB/FPB-B modules, the remaining exons encode the N-terminal amino acids and C-terminal array of zinc finger units, respectively.     

Characterization of two novel KRAB-domain-containing zinc finger genes, ZNF460 and ZNF461, on human chromosome 19q13.1-->q13.4

This study reports the cloning and characterization of two novel human zinc finger protein cDNAs (ZNF460 and ZNF461) from a fetal brain cDNA library. The ZNF460 cDNA is 3,135 bp in length encoding a 562-amino-acid polypeptide and the ZNF461 cDNA is 2,548 bp encoding a 563-amino-acid protein. Both of the proteins contain a KRAB A+B box and eleven C2H2 type zinc finger motifs. ZNF461 shows high similarity with the rat GIOT-1 gene (GIOT1). The ZNF460 gene mapped to 19q13.4 with 3 exons, and ZNF461 mapped to 19q13.1 with 6 exons. Both of the two genes are ubiquitously expressed in normal human tissues and the abundance of the ZNF460 mRNA is relatively low.     

Linkage of atopic dermatitis to chromosomes 4q22, 3p24 and 3q21

Atopic dermatitis (AD) is a common, itchy skin disease of complex inheritance characterized by dermal and epidermal inflammation. The heritability is considerable and well documented. To date, four genome scans have examined the AD phenotype, showing replicated linkage at 3p26-22, 3q13-21 and 18q11-21. Our previous AD scan showed evidence of linkage to loci at 3p and 18q, and furthermore at 4p15-14. In order to further investigate the genetic basis of AD, we collected and analysed a new Danish family sample consisting of 130 AD sib pair families (555 individuals including 295 children with AD). AD was diagnosed after clinical examination, AD severity was scored and specific IgE was determined. A linkage scan of chromosome 3, 4 and 18 was performed using 91 microsatellite markers. Linkage analyses were performed of dichotomous phenotypes and semi-quantitative traits including the AD severity score. We analysed the novel AD sample alone and together with the previously examined sample. AD severity showed a maximum Z-score of 3.7 at 4q22.1 suggesting the localization of a novel gene for AD severity. A maximum MOD score of 4.6 was obtained at 3p24 for the AD phenotype, providing the first significant linkage of AD at this locus. A maximum MLS score of 3.3 was obtained at 3q21 for IgE-associated AD, and evidence of linkage was also obtained at 3p22.2-21.31, 3q13, 4q35, and 18q12. The results presented should provide a firm basis for gene-targeting studies of AD and related disorders.     

Positional clustering of differentially expressed genes on human chromosomes 20, 21 and 22

Background  

Clusters of genes co-expressed are known in prokaryotes (operons) and were recently described in several eukaryote organisms, including Human. According to some studies, these clusters consist of housekeeping genes, whereas other studies suggest that these clustered genes exhibit similar tissue specificity. Here we further explore the relationship between co-expression and chromosomal co-localization in the human genome by analyzing the expression status of the genes along the best-annotated chromosomes 20, 21 and 22.     

The zinc finger proteins ZC3H20 and ZC3H21 stabilise mRNAs encoding membrane proteins and mitochondrial proteins in insect-form Trypanosoma brucei

ZC3H20 and ZC3H21 are related trypanosome proteins with two C(x)₈C(x)₅C(x)₃H zinc finger motifs. ZC3H20 is present at a low level in replicating mammalian-infective bloodstream forms, but becomes more abundant when they undergo growth arrest at high density; ZC3H21 appears only in the procyclic form of the parasite, which infects Tsetse flies. Each protein binds to several hundred mRNAs, with overlapping but not identical specificities. Both increase expression of bound mRNAs, probably through recruitment of the MKT1-PBP1 complex. At least 28 of the bound mRNAs decrease after depletion of ZC3H20, or of ZC3H20 and ZC3H21 together; their products include procyclic-specific proteins of the plasma membrane and energy metabolism. Simultaneous depletion of ZC3H20 and ZC3H21 causes procyclic forms to shrink and stop growing; in addition to decreases in target mRNAs, there are other changes suggestive of loss of developmental regulation. The bloodstream-form-specific protein RBP10 controls ZC3H20 and ZC3H21 expression. Interestingly, some ZC3H20/21 target mRNAs also bind to and are repressed by RBP10, allowing for dynamic regulation as RBP10 decreases and ZC3H20 and ZC3H21 increase during differentiation.     

Translocation between chromosome 7 and chromosome 22, t(7;22)(p22;q12), in a patient with chronic myelocytic leukemia

Summary A 46-year-old man with chronic myelocytic leukemia had a new variant translocation between chromosome 22 and chromosome 7 in bone marrow cells. No involvement of chromosome 9 was seen. The patient entered blastic transformation within half a year, by which time he had acquired an isochromosome 17 in addition to the variant translocation.     

Chromosome mapping of the human RAS-related RAP1A, RAP1B, and RAP2 genes to chromosomes 1p12----p13, 12q14, and 13q34, respectively

Three human cDNAs encoding new RAS-related cDNAs, designated RAP1A, RAP1B, and RAP2, have been isolated previously. The encoded proteins are highly related to RAS in the effector region and share an overall identity with RAS of approximately 50%. Using the complete cDNAs or parts thereof as probes, each RAP gene has been localized on human chromosomes by in situ hybridization. The three genes RAP1A, RAP1B, and RAP2 have been assigned to chromosome bands 1p12----p13, 12q14, and 13q34, respectively.     

Human inner ear OCP2 cDNA maps to 5q22-5q35.2 with related sequences on chromosomes 4p16.2-4p14, 5p13-5q22, 7pter-q22, 10 and 12p13-12qter

Mouse Ocp2-rs2 maps to chromosome 11 and encodes an 18.6 kDa peptide abundantly expressed in the organ of Corti. We show that sequences similar to murine Ocp2-rs2 are found on human chromosomes 4p16.2-4p14, 5p13-5q35.2, 7pter-q22, 10 and 12p13-12qter as revealed by Southern blot analyses of human/rodent somatic cell hybrids. A fetal human inner ear cDNA library was screened with a cloned 254 bp PCR product of murine Ocp2-rs2. One of two human cDNA clones (CM1) was sequenced from the 5′ end that begins with murine Ocp2-rs2 codon 14 through the stop codon and 258 nucleotides of 3′-UTR and was found to have the identical deduced amino acid sequence to Ocp2-rs2. Based on the sequence in the 3′-UTR of CM1, a PCR primer pair was synthesized and used to confirm that a human homologue of Ocp2-rs2, designated OCP2 and expressed in the developing human inner ear, is localized to 5q22-5q35.2. Other OCP2-like sequences located on chromosomes 4p16.2-4p14, 7pter-q22 and 12p13-12qter (but not the chromosome 10 OCP2-like sequence) will PCR amplify the expected size product at a lower annealing temperature using the OCP2 3′-UTR PCR primers indicating that there may be a human OCP2 gene family.     

Localization of the human phosphotyrosine phosphatase-related genes (h-PRL-1) to chromosome bands 1p35–p34, 17q12–q21, 11q24–q25 and 12q24

The h-PRL-1 gene codes for a new phosphotyrosine phosphatase that may play an important role in the control of basic cellular processes such as cell growth and proliferation. Using the cDNA of the h-PRL-1 gene as a probe, we examined a somatic mouse and hamster × human hybrid panel and found that chromosomes 1, 17 and 11 harbor sequences homologous to h-PRL-1. By in situ hybridization of metaphase spreads, subchromosomal localizations were determined at bands 1p35–p34, 17q12– q21 and 11q24–q25; in addition, a faint signal was detected at 12q24. The chromosomal assignment of the genes homologous to h-PRL-1 will help the investigation of its possible involvement in human diseases involving genetic alteration at these chromosomal regions. Received: 12 June 1996 / Revised: 27 July 1996     

Localization of PGI (biglycan, BGN) and PGII (decorin, DCN, PG-40) genes on human chromosomes Xq13-qter and 12q, respectively

The genes for PGI (biglycan, BGN) and PGII (decorin, DCN) have been assigned to human chromosomes X and 12 by Southern analysis of a panel of human-rodent somatic cell hybrid DNAs with cDNA probes for these related small proteoglycans. Regional localization of BGN to Xq13-qter and DCN to 12p12.1-qter was also obtained by examining hybrids containing spontaneous breaks or well-characterized translocations involving chromosomes X and 12. Biglycan (BGN) is a single-copy gene about 6 kb in length. Hybridization with subfragment cDNA probes suggests the presence of two copies of the decorin (DCN) gene, or related sequences, at the locus on chromosome 12, although there is no evidence for function of more than one DCN gene. Efforts to detect restriction fragment length polymorphisms with these probes were unsuccessful.