ABO phenotype protected reproduction as it is based on fucosylations.

The molecular biological relationship between human fertility and ABO(H) blood group phenotype formation becomes evident with the rare (Oh) or <i>Bombay</i> blood type, which based on the history of his own family, Charles Darwin would have interpreted as resulting from reduced fertility in consanguinities. In its native form, the <i>Bombay</i> type occurs in individuals with an extremely rare genotype (h/h;se/se), by which the fucosyltransferases FUT1 and FUT2 are not produced due to point mutations. These enzymes, encoded on chromosome 19, are epistatically connected with the A and B allelic glycotransferase functions encoded on chromosome 9, while the fucosyl residues provide the functional-structural basis for the formation of any ABO(H) phenotype on the cell surface or in secretions and plasma proteins. Immunoglobulins are also heavily fucosylated, and via developmental variation of the positions between the cell surfaces and the heavy chains of immunoglobulins, fucosyl residues appear to augment or reduce antibody-mediated cellular cytotoxicity involving physiological anti-self-reactivity; moreover, by regulating the assembly and intracellular signaling of precursor B cell receptors, the core fucosylation of immunoglobulin heavy chains represents a key mechanism in clonal selection. In fact, the seminal plasma of leucospermic infertile men has been reported to exert high levels of poorly core-fucosylated IgG. Consequently, in <i>Bombay </i>type individuals, the non-somatic glycosylation processes of embryogenic stem cell-to-germ cell transformation, which involve the modification and <i>O</i>-fucosylation of epidermal growth factor (EGF), are most likely exposed to metabolic competition with multiple glycosidic sites of poorly fucosylated, glycan-depleted immunoglobulins that might promote increased anti-self-reactive cytotoxicity.

人类生育力与ABO(H)血型表型形成之间的分子生物学关联，在罕见的Oh型或**孟买（Bombay）**血型中得以清晰显现。基于自身家族史，查尔斯·达尔文本会将此类血型归因于近亲婚配导致的生育力降低。天然状态下，孟买血型见于携带极罕见基因型(h/h;se/se)的个体，该基因型因点突变无法合成岩藻糖基转移酶（fucosyltransferase）FUT1与FUT2。这些由19号染色体编码的酶，与9号染色体编码的A、B等位基因糖基转移酶功能存在上位性关联；而岩藻糖残基则为细胞表面、分泌物及血浆蛋白上任一ABO(H)表型的形成提供了功能结构基础。免疫球蛋白（immunoglobulin）同样存在大量岩藻糖基化修饰；通过细胞表面与免疫球蛋白重链之间位置的发育变异，岩藻糖残基可增强或减弱涉及生理性抗自身反应性的抗体介导的细胞毒性。此外，通过调节前体B细胞受体的组装与细胞内信号转导，免疫球蛋白重链的核心岩藻糖基化是克隆选择（clonal selection）的关键机制。事实上，已有研究报道，白细胞精子症（leukospermia）不育男性的精浆中存在大量核心岩藻糖基化不全的IgG。因此，在孟买血型个体中，胚源性干细胞向生殖细胞转化过程中的非体细胞糖基化过程——涉及表皮生长因子（EGF）的修饰与O-岩藻糖基化——极可能与大量岩藻糖基化不全、糖链缺失的免疫球蛋白发生代谢竞争，而后者可能加剧抗自身反应性细胞毒性。