Evolutionary conflicts in pregnancy and calcium metabolism - A review

被引:32
作者
Haig, D [1 ]
机构
[1] Harvard Univ, Dept Organism & Evolut Biol, Cambridge, MA 02138 USA
关键词
D O I
10.1016/j.placenta.2004.01.006
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
The maternal-fetal unit contains three distinct haplotypes at each locus: the maternally derived fetal haplotype (MDFH) that is shared by the mother and fetus, the paternally derived fetal haplotype (PDFH), and the non-inherited maternal haplotype (NIMH). The evolutionary forces acting on these haplotypes are distinct. The NIMH is absent from the offspring and could benefit from early abortion if this enhances the probability of the mother conceiving again and producing an offspring that inherits the NIMH. This raises the possibility that some forms of recurrent spontaneous abortion may be caused by non-inherited haplotypes. Such 'selfish' behaviour would be opposed by other components of the maternal genome. Natural selection acting on genes expressed in fetuses (or their placentae) favours greater maternal investment in the fetus than does natural selection acting on genes expressed in mothers. Furthermore, in the presence of genomic imprinting, the PDFH favours greater levels of investment in the fetus than does the MDFH. These conflicts are illustrated using the example of maternal-fetal conflicts over the supply of calcium. Inactivation of the paternal copy of GNAS in proximal renal tubule is interpreted as a measure to maintain fetal bone mineralization in times of calcium stress at the expense of the maternal skeleton. (C) 2004 IFPA and Elsevier Ltd. All rights reserved.
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页码:S10 / S15
页数:6
相关论文
共 46 条
[1]   INTRAUTERINE HYPERPARATHYROIDISM - A COMPLICATION OF UNTREATED MATERNAL HYPOPARATHYROIDISM [J].
ACETO, T ;
BATT, RE ;
BRUCK, E ;
SCHULTZ, RB ;
PEREZ, YR .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1966, 26 (05) :487-+
[2]  
Aldred MA, 2000, HUM MUTAT, V16, P183, DOI 10.1002/1098-1004(200009)16:3<183::AID-HUMU1>3.0.CO
[3]  
2-L
[4]  
[Anonymous], 2002, Genomic Imprinting and Kinship
[5]   Paternal uniparental isodisomy of chromosome 20q -: and the resulting changes in GNAS1 methylation -: as a plausible cause of pseudohypoparathyroidism [J].
Bastepe, M ;
Lane, AH ;
Yüppner, H .
AMERICAN JOURNAL OF HUMAN GENETICS, 2001, 68 (05) :1283-1289
[6]  
BRINGHURST FR, 1995, ENDOCRINOLOGY, P1015
[7]   An inherited mutation associated with functional deficiency of the α-subunit of the guanine nucleotide-binding protein Gs in pseudo- and pseudohypoparathyroidism [J].
Fischer, JA ;
Egert, F ;
Werder, E ;
Born, W .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1998, 83 (03) :935-938
[8]  
FRIEDMAN PA, 2000, KIDNEY PHYSL PATHOPH, V2, P1749
[9]   PREGNANCY AS STATE OF PHYSIOLOGICAL ABSORPTIVE HYPERCALCIURIA [J].
GERTNER, JM ;
COUSTAN, DR ;
KLIGER, AS ;
MALLETTE, LE ;
RAVIN, N ;
BROADUS, AE .
AMERICAN JOURNAL OF MEDICINE, 1986, 81 (03) :451-456
[10]   GENETIC CONFLICTS IN HUMAN-PREGNANCY [J].
HAIG, D .
QUARTERLY REVIEW OF BIOLOGY, 1993, 68 (04) :495-532