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Human Molecular Genetics Pages 667-671  

Genetic mapping of a maternal locus responsible for familial hydatidiform moles
Introduction
Results
   Establishment of linkage
   Genetic mapping and haplotype analysis
Discussion
Materials And Methods
   Families
   Genotyping
   Linkage analyses
Acknowledgements
References

Genetic mapping of a maternal locus responsible for familial hydatidiform moles

Genetic mapping of a maternal locus responsible for familial hydatidiform moles

Yolla Bou Moglabey1, Renate Kircheisen3, Muhieddine Seoud2, Nisrine El Mogharbel1, Ignatia Van den Veyver4 and Rima Slim1,*

1Department of Biochemistry and 2Department of Obstetrics and Gynecology, American University of Beirut, PO Box 11-236, Beirut, Lebanon, 3Institut für Klinische Genetik, Mainz, Germany and 4Departments of Obstetrics and Gynecology and of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA

Received November 20, 1998; Revised and Accepted January 19, 1999

Hydatidiform mole (HM) is the product of an aberrant human pregnancy in which there is an abnormal embryonic development and proliferation of placental villi. The incidence of HM varies between ethnic groups, and occurs in 1 in every 1500 pregnancies in the USA. All HM cases are sporadic, except for extremely rare familial cases. The exact mechanisms leading to molar pregnancies are unknown. We previously postulated that women with recurrent hydatidiform moles are homozygous for an autosomal recessive defective gene. To map this gene genetically, we initiated a genome-wide scan with highly polymorphic short tandem repeats in individuals from two families with recurrent HM. Here, we demonstrate that a defective maternal gene is responsible for recurrent HM. This gene resides on chromosome 19q13.3-13.4 in a 15.2 cM interval flanked by D19S924 and D19S890. The identification of a gene for HM adds new insights into the molecular genetics of early embryogenesis and may be relevant to the large number of patients with sporadic HM.

INTRODUCTION

Hydatidiform mole (HM) (MIM 231909), the most common form of gestational trophoblastic neoplasia, is characterized by atypical proliferation of placental villi and absence of, or abnormal, embryonic development (1,2). Based on histology and karyotype data, HMs are divided into two types: complete hydatidiform moles (CHMs) and partial hydatidiform moles (PHMs). The complete forms have general trophoblastic proliferation, and usually lack an embryo and amniotic membranes. However, remnant embryonic structures and inner cell mass derivatives are now found in some cases of CHM evacuated at an early stage (3). CHMs usually have a diploid genome, and are androgenetic in at least 80% of cases (4,5). Among the androgenetic CHMs, 60% are monospermic (with one identical set of paternal chromosomes) and 20% are dispermic (with two different sets of paternal chromosomes). The remaining 20% have a biparental genomic contribution to the molar tissues (5). PHMs are characterized by focal trophoblastic proliferation. Embryos and amniotic membranes are usually present in these molar pregnancies, and they are usually triploid, with two sets of paternal chromosomes and one set of maternal chromosomes (1,2). Sporadic HMs are common and occur in ~1 in every 1500 pregnancies in the USA, with PHMs constituting up to 50% of these cases. This incidence varies between ethnic groups and reaches 1 in every 250 pregnancies in Eastern Asia (1,2). The exact etiology of HM is unknown. Phenotype-genotype comparison between androgenetic CHMs and PHMs indicates that both maternally and paternally imprinted genes play a role in the pathophysiology of molar pregnancies.

Familial cases of HM are extremely rare. So far, only seven familial cases have been reported (6-10). In six of these cases, the molar pregnancies are of the CHM type, and none of them has been studied at the molecular level (6-9). Previously, we described a consanguineous Lebanese family in which two members had recurrent CHM (10) and one member had recurrent PHM (11,12). We demonstrated that these molar pregnancies are diploid, and have a biparental contribution to their genomes (M.N. Helwani, M. Seoud, L. Zahed, G. Zaatari, A. Khalil and R. Slim, manuscript in preparation). Based on our data, and on previously reported familial HM cases, we postulated that women with recurrent HM are homozygous for an autosomal recessive mutation (M.N.Helwani et al., manuscript in preparation).

To map this gene genetically, we performed a genome-wide scan on the Lebanese family and on a previously reported German family in which three sisters had a total of eight molar pregnancies. Here we demonstrate that a maternal gene is responsible for familial recurrent HM. This gene maps to chromosome 19q13.3-13.4 in a 15.2 cM genetic interval flanked by D19S924 and D19S890.

RESULTS

Establishment of linkage

To map the gene responsible for HM, we carried out a genome-wide scan with highly polymorphic short tandem repeats (13) on DNAs from 11 individuals, seven members from the Lebanese family MoLb1 (members 1, 2, 4, 5, 6, 7 and 8 in Fig. 1) and four members from the German family MoGe2 (members 1, 2, 3 and 4). After excluding linkage to 60% of the genome, the first marker to demonstrate homozygosity in the three affected members of family MoLb1 was D19S926. This marker surprisingly was also homozygous in the three affected members of family MoGe2 and gave a cumulative lod score of 2.91 at [thetas] = 0. Additional markers from this region (13) were then analyzed on DNA from the previously genotyped members and from five additional members, two from family MoLb1 (3 and 9) and three from family MoGe2 (5, 6 and 7). Lod scores >3.0 were obtained at [thetas] = 0 for the most informative markers D19S418 (Zmax = 3.26), D19S877 (Zmax = 3.20), D19S404 (Zmax = 3.71), D19S210 (Zmax = 3.98) and D19S214 (Zmax = 3.60) (Table 1).


Figure 1. Pedigree structure of HM families, MoLb1 and MoGe2, showing the most likely haplotypes for 19q13.3-13.4 markers. Affected individuals are designated as filled black symbols, unaffected subjects as unfilled symbols, and individuals with unknown phenotype are shown as gray symbols. Common haplotypes segregating with the disease phenotype are boxed. Marker order was determined from the Généthon genetic map (13).

Genetic mapping and haplotype analysis

Haplotypes were established by minimizing the number of recombination events for 17 microsatellite markers from chromosome 19qter (Fig. 1). The three affected members of the consanguineous Lebanese family share a common homozygous region, by descent, at 12 adjacent markers spanning a 12.4 cM interval, whereas their unaffected first-degree relatives (members 1 and 7) are heterozygous. Also, the three affected members of family MoGe2 share a homozygous region at 12 adjacent markers, while their unaffected mother is heterozygous. The presence of this large homozygous region in the three affected members of family MoGe2 was not expected since no blood relationship between the parents was reported by the family members. However, the two parents originate from a small rural region and probably have inherited the same rare mutation from a single ancestor.

Our data indicate that women with familial recurrent HM are homozygous for an autosomal recessive mutation. The defective gene lies on human chromosome 19q13.3-13.4 within a 15.2 cM interval flanked by the loci D19S924 and D19S890 (Fig. 2).

DISCUSSION

We mapped a maternal locus for HM at the telomeric region of chromosome 19q using a combination of linkage search through the genome and homozygosity analysis. Two-point lod scores >3.0 were obtained at [thetas] = 0 between the disease phenotype and five microsatellite marker loci from 19q13.3-13.4. Haplotype and homozygosity analyses map the HM gene to a 15.2 cM interval flanked by D19S924 and D19S890 (Fig. 2).

Table 1. Pairwise lod score between microsatellite markers and molar pregnancies
Locus Family [thetas] Zmax [thetas]max
0.00 0.1 0.2 0.3 0.4
D19S924 MoLb1 -[infin] -0.73 -0.22 -0.05 0.00 0.00 0.5
MoGe2 -[infin] 0.02 0.12 0.09 0.03 0.12 0.2
Total -[infin] -0.71 -0.10 0.04 0.03 0.12 0.2
D19S418 MoLb1 2.37 1.87 1.34 0.80 0.31 2.37 0.00
MoGe2 0.89 0.67 0.44 0.23 0.06 0.89 0.00
Total 3.26 2.54 1.78 1.03 0.37 3.26 0.00
D19S926 MoLb1 2.35 1.85 1.30 0.73 0.22 2.35 0.00
MoGe2 0.60 0.46 0.32 0.17 0.05 0.60 0.00
Total 2.95 2.31 1.62 0.90 0.27 2.95 0.00
D19S877 MoLb1 2.60 2.08 1.54 0.97 0.42 2.60 0.00
MoGe2 0.60 0.46 0.31 0.17 0.04 0.60 0.00
Total 3.20 2.54 1.85 1.14 0.46 3.20 0.00
D19S404 MoLb1 3.11 2.57 1.96 1.30 0.62 3.11 0.00
MoGe2 0.60 0.46 0.32 0.17 0.05 0.60 0.00
Total 3.71 3.03 2.28 1.47 0.67 3.71 0.00
D19S210 MoLb1 3.12 2.58 1.97 1.31 0.62 3.12 0.00
MoGe2 0.86 0.65 0.43 0.22 0.06 0.86 0.00
Total 3.98 3.23 2.40 1.53 0.68 3.98 0.00
D19S214 MoLb1 2.40 1.91 1.38 0.82 0.32 2.40 0.00
MoGe2 1.20 0.93 0.64 0.34 0.10 1.20 0.00
Total 3.60 2.84 2.02 1.16 0.42 3.60 0.00
D19S890 MoLb1 -2.00 1.14 0.96 0.65 0.31 1.14 0.10
MoGe2 1.20 0.46 0.64 0.34 0.10 1.20 0.00
Total -0.80 1.60 1.60 0.99 0.41 2.24 0.05


Figure 2. Schematic diagram showing part of chromosome 19q13.3-13.4 and the relative position of the markers used in this region (13). The distances are in centiMorgans. The bold segment denotes the HM candidate region.

Numerous genes have so far been mapped to 19q13.3-13.4. Of these, the most interesting candidates to test for mutations in women with HM are several Krüppel-type (C2H2) zinc finger-containing genes clustered in the distal part of the HM critical region (14,15). These genes code for transcriptional factors known to be expressed in many human cell lines of different embryological derivation. In Drosophila, the Krüppel genes are the first zygotic genes to be activated by maternal transcription factors, and play an important role in very early embryogenesis (16). One of these zinc finger-containing genes, PEG3, for paternally expressed gene, is maternally imprinted in mice (17,18). In humans, PEG3 is transcribed in many tissues, with the highest levels in ovary and placenta, while in mice the highest level was found in adult brain (18). The function of this imprinted gene is unknown as yet. However, it has been demonstrated recently that Peg3 participates in the tumor necrosis factor (TNF)-NF[kappa]B signal transduction pathway, which regulates cell proliferation, differentiation and programmed cell death (19).


Most of the imprinted genes identified so far are clustered together (20). Within these clusters, maternally and paternally imprinted genes are interspersed over several hundred kilobases. Therefore, the presence in 19q13.3-13.4 of the human homolog of Peg3 is in favor of the existence of additional maternally and paternally imprinted genes in this region. Furthermore, the mouse homologous region of the human 19q13.3-13.4 maps to two linkage groups on the mouse chromosome 7 and to a small region on the proximal part of the mouse chromosome 17 (21). These three regions fail to show genetic complementation in intercrosses of heterozygotes for reciprocal translocations (22,23), thereby supporting again the presence of imprinted genes in 19q13.3-13.4. The mapping of the HM gene to a region suggested to harbor imprinted genes is consistent with their involvement in the etiology of HM. However, our data indicate that the molar pregnancies in our families have resulted from the disruption of a single gene. We therefore suggest thatthe defective maternal gene in the two families regulates the expression of several imprinted genes in 19qter during early embryogenesis. Our hypothesis is in agreement with the proposal that maternal imprinting occurs during oocyte growth and that its disruption leads to a modified expression of paternally and maternally imprinted genes during embryogenesis (24).

We hereby describe the first genetic mapping of a maternal locus involved in early embryogenesis in mammals. The identification of this gene will help in understanding the exact mechanisms leading to molar pregnancies and may provide further insights into the understanding of the imprinting process and its role in early embryonic development.

MATERIALS AND METHODS

Families

Blood samples from two previously published families (Fig. 1), MoLb1 and MoGe2, having patients with recurrent HM were collected with the informed consent of all subjects. MoLb1 is a consanguineous family of Lebanese origin in which two sisters and their cousin had recurrent HM. Member 4 (in MoLb1) had eight CHM, five abortions and no normal pregnancy; member 6 had five CHM, two abortions and one normal pregnancy (M.N.Helwani et al., manuscript in preparation); and member 8 had four PHM and two normal pregnancies (11,12). MoGe2 is of German origin, and no blood relationship is reported between the parents. Only female siblings of MoLb1 were included. The phenotype was classified as affected for females with at least one molar pregnancy (members 4, 6 and 8 in family MoLb1 and members 2, 3 and 4 in family MoGe2), unaffected for women who had only normal pregnancies (members 1, 3 and 7 in MoLb1 and member 1 in MoGe2 ) and unknown for females who had never been pregnant (members 5 and 9 in MoLb1 and members 5, 6 and 7 in MoGe2). Member 6 of family MoGe2 has never been pregnant despite infertility treatment for several years, and her diagnosis was kept as unknown. The diagnosis of HM was based on histological examinations as previously described (10-12).

Genotyping

DNA was extracted from total blood according to standard procedures. Genome-wide screening was performed with a panel of 250 microsatellite markers spaced at 10-15 cM intervals (13). The average marker heterozygosity was 0.79. Microsatellite markers were typed by PCR. The PCR products were separated in 6% polyacrylamide (6 M urea) gels and transferred onto membranes (N+; Amersham). For each PCR, one of the primers was end-labeled with [[alpha]-32P]dCTP and hybridized to the membrane. All markers were scored independently by two observers.

Linkage analyses

Linkage analyses were performed using the Linkage Control Package program (version 5.1) (25). Full penetrance was assumed with a disease allele frequency of 0.00002. For the analysis of the Lebanese family, allele frequencies at all markers located between D19S924 and D19S890 were calculated from 44 unrelated Lebanese individuals. For the other markers and for family MoGe2, published allele frequencies in the Caucasian population were used (http://gdbwww.gdb.org/gdb/ ). New alleles were detected in the Lebanese population at most of the analyzed loci (data available upon request).

ACKNOWLEDGEMENTS

We thank the family members for their cooperation; Drs Kolkmann and Beckert for providing pathological samples; Drs Schnabel and Sinn for helpful discussions; and Professor I. Durr for his continuous support. This work was supported by the Medical Practice Plan and the University Research Board of the American University of Beirut.

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*To whom correspondence should be addressed. Tel: +961 1 353 465; Fax: +961 1 744 464; Email: rslim@aub.edu.lb

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