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Male-mediated prenatal loss: Functions and mechanisms.

ABSTRACT: Sexually selected infanticide has been the subject of intense empirical and theoretical study for decades; a related phenomenon, male-mediated prenatal loss, has received much less attention in evolutionary studies. Male-mediated prenatal loss occurs when inseminated or pregnant females terminate reproductive effort following exposure to a nonsire male, either through implantation failure or pregnancy termination. Male-mediated prenatal loss encompasses two sub-phenomena: sexually selected feticide and the Bruce effect. In this review, we provide a framework that explains the relationship between feticide and the Bruce effect and describes what is known about the proximate and ultimate mechanisms involved in each. Using a simple model, we demonstrate that male-mediated prenatal loss can provide greater reproductive benefits to males than infanticide. We therefore suggest that, compared to infanticide, male-mediated prenatal loss may be more prevalent in mammalian species and may have played a greater role in their social evolution than has previously been documented.

SUBMITTER: Zipple MN

PROVIDER: S-EPMC6548597 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature

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Male-mediated prenatal loss: Functions and mechanisms.

Zipple Matthew N MN Roberts Eila K EK Alberts Susan C SC Beehner Jacinta C JC

Evolutionary anthropology 20190406 3

Sexually selected infanticide has been the subject of intense empirical and theoretical study for decades; a related phenomenon, male-mediated prenatal loss, has received much less attention in evolutionary studies. Male-mediated prenatal loss occurs when inseminated or pregnant females terminate reproductive effort following exposure to a nonsire male, either through implantation failure or pregnancy termination. Male-mediated prenatal loss encompasses two sub-phenomena: sexually selected fetic ...[more]

PMID: 30953577

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Project description:BACKGROUND: Mutations in the coding region of angiogenin (ANG) gene have been found in patients suffering from Amyotrophic Lateral Sclerosis (ALS). Neurodegeneration results from the loss of angiogenic ability of ANG (protein coded by ANG). In this work, we performed extensive molecular dynamics (MD) simulations of wild-type ANG and disease associated ANG variants to elucidate the mechanism behind the loss of ribonucleolytic activity and nuclear translocation activity, functions needed for angiogenesis. METHODOLOGY/PRINCIPAL FINDINGS: MD simulations were carried out to study the structural and dynamic differences in the catalytic site and nuclear localization signal residues between WT-ANG (Wild-type ANG) and six mutants. Variants K17I, S28N, P112L and V113I have confirmed association with ALS, while T195C and A238G single nucleotide polymorphisms (SNPs) encoding L35P and K60E mutants respectively, have not been associated with ALS. Our results show that loss of ribonucleolytic activity in K17I is caused by conformational switching of the catalytic residue His114 by 99°. The loss of nuclear translocation activity of S28N and P112L is caused by changes in the folding of the residues (31)RRR(33) that result in the reduction in solvent accessible surface area (SASA). Consequently, we predict that V113I will exhibit loss of angiogenic properties by loss of nuclear translocation activity and L35P by loss of both ribonucleolytic activity and nuclear translocation activity. No functional loss was inferred for K60E. The MD simulation results were supported by hydrogen bond interaction analyses and molecular docking studies. CONCLUSIONS/SIGNIFICANCE: Conformational switching of catalytic residue His114 seems to be the mechanism causing loss of ribonucleolytic activity and reduction in SASA of nuclear localization signal residues (31)RRR(33) results in loss of nuclear translocation activity in ANG mutants. Therefore, we predict that L35P mutant, would exhibit loss of angiogenic functions, and hence would correlate with ALS while K60E would not show any loss.

Dataset Information

Male-mediated prenatal loss: Functions and mechanisms.

Publications

Male-mediated prenatal loss: Functions and mechanisms.

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