GENETIC CONFLICTS IN HUMAN-PREGNANCY

被引:732
作者
HAIG, D
机构
关键词
D O I
10.1086/418300
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Pregnancy has commonly been viewed as a cooperative interaction between a mother and her fetus. The effects of natural selection on genes expressed in fetuses, however, may be opposed by the effects of natural selection on genes expressed in mothers. In this sense, a genetic conflict can be said to exist between maternal and fetal genes. Fetal genes will be selected to increase the transfer of nutrients to their fetus, and maternal genes will be selected to limit transfers in excess of Soma maternal optimum. Thus a process of evolutionary escalation is predicted in which fetal actions are opposed by maternal countermeasures. The phenomenon of genomic imprinting means that a similar conflict exists within fetal cells between genes that are expressed when maternally derived, and genes that are expressed when paternally derived. During implantation, fetally derived cells (trophoblast) invade the maternal endometrium and remodel the endometrial spiral arteries into low-resistance vessels that are unable to constrict. This invasion has three consequences. First, the fetus gains direct access to its mother's arterial blood. Therefore, a mother cannot reduce the nutrient content of blood reaching the placenta without reducing the nutrient supply to her own tissues. Second, the volume of blood reaching the placenta becomes largely independent of control by the local maternal vasculature. Third, the placenta is able to release hormones and other substances directly into the maternal circulation. Placental hormones, including human chorionic gonadotropin (hCG) and human placental lactogen (hPL), are predicted to manipulate maternal physiology for fetal benefit. For example, hPL is proposed to act on maternal prolactin receptors to increase maternal resistance to insulin. If unopposed, the effect of hPL would be to maintain higher blood glucose levels for longer periods after meals. This action, however, is countered by increased maternal production of insulin. Gestational diabetes develops if the mother is unable to mount an adequate response to fetal manipulation. Similarly, fetal genes are Predicted to enhance the flow of maternal blood through the placenta by increasing maternal blood pressure. Preeclampsia can be interpreted as an attempt by a poorly nourished fetus to increase its supply of nutrients by increasing the resistance of its mother's peripheral circulation.
引用
收藏
页码:495 / 532
页数:38
相关论文
共 346 条
  • [1] Amoroso EC., 1952, MARSHALLS PHYSL REPR, VII
  • [2] IMMUNOHISTOCHEMICAL DEMONSTRATION OF PLACENTAL HORMONES IN THE DIAGNOSIS OF UTERINE VERSUS ECTOPIC PREGNANCY
    ANGEL, E
    DAVIS, JR
    NAGLE, RB
    [J]. AMERICAN JOURNAL OF CLINICAL PATHOLOGY, 1985, 84 (06) : 705 - 709
  • [3] APLIN JD, 1988, CELL TISSUE RES, V253, P231
  • [4] GLYCOPROTEIN GLYCOSYLATION AND THE IMMUNOSUPPRESSIVE EFFECTS OF HUMAN-PREGNANCY SERUM
    ARKWRIGHT, P
    RADEMACHER, T
    MARSHALL, J
    DWEK, R
    REDMAN, C
    [J]. JOURNAL OF REPRODUCTIVE IMMUNOLOGY, 1992, 21 (01) : 97 - 102
  • [5] BEHAVIOR OF HPL AND GH PLASMATIC RATE IN PREGNANT-WOMEN AT DIFFERENT TIMES OF THEIR PREGNANCY DURING DYNAMIC TESTS
    ARTENISIO, AC
    VOLPE, A
    RAGONESE, F
    MACCARRONE, G
    FORTE, F
    CONSOLO, F
    [J]. HORMONE AND METABOLIC RESEARCH, 1980, 12 (05) : 205 - 208
  • [6] APPLICATION OF GENE AMPLIFICATION BY POLYMERASE CHAIN-REACTION TO GENETIC-ANALYSIS OF MOLAR MITOCHONDRIAL-DNA - THE DETECTION OF A NUCLEAR EMPTY OVUM AS THE CAUSE OF COMPLETE MOLE
    AZUMA, C
    SAJI, F
    TOKUGAWA, Y
    KIMURA, T
    NOBUNAGA, T
    TAKEMURA, M
    KAMEDA, T
    TANIZAWA, O
    [J]. GYNECOLOGIC ONCOLOGY, 1991, 40 (01) : 29 - 33
  • [7] HEMODYNAMICS AT REST AND DURING EXERCISE IN NORMAL PREGNANCY AS STUDIED BY CARDIAC CATHETERIZATION
    BADER, RA
    BADER, ME
    ROSE, DJ
    BRAUNWALD, E
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1955, 34 (10) : 1524 - 1536
  • [8] PLATELET ANGIOTENSIN-II BINDING AND PLASMA-RENIN CONCENTRATION, PLASMA-RENIN SUBSTRATE AND PLASMA ANGIOTENSIN-II IN HUMAN-PREGNANCY
    BAKER, PN
    PIPKIN, FB
    SYMONDS, EM
    [J]. CLINICAL SCIENCE, 1990, 79 (04) : 403 - 408
  • [9] PLATELET ACTIVATION AND VASCULAR DAMAGE IN GESTATIONAL HYPERTENSION
    BALLEGEER, VC
    SPITZ, B
    DEBAENE, LA
    VANASSCHE, AF
    HIDAJAT, M
    CRIEL, AM
    [J]. AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1992, 166 (02) : 629 - 633
  • [10] BAMBRA CS, 1984, J REPROD FERTIL, V71, P227, DOI 10.1530/jrf.0.0710227