Delaunay J, Alloisio N, Morle L, Baklouti F, Dalla Venezia N, Maillet P, Wilmotte R
Laboratoire de Génétique Moléculaire Humaine, CNRS URA 1171, Institut Pasteur de Lyon, France.
Ann Genet. 1996;39(4):209-21.
Red cells ow their mechanical properties, that is, their resistance and their elastic deformability, to a protein network that laminates the lipid bilayer and to proteins spanning the latter. All proteins are interconnected. Their structure, as well as the structure of the corresponding genes, will be outlined. Numerous mutations have allowed to reclassify hereditary elliptocytosis (HE) and poikilocytosis (HP), and, more recently, hereditary spherocytosis (HS) into well defined subsets of hereditary hemolytic anemias. HE stems from changes in the SPTA1, SPTB, EL1 and (exceptionally) GPYC genes that encode spectrin alpha- and beta- chains, protein 4.1 and glycophorin C/D, respectively. HS derives from altercations in the ANK1, EPB3 and ELB42 genes, encoding ankyrin, band 3 and protein 4.2, respectively, and also in the SPTA1 and SPTB genes. We will present a repertory of the known mutations. Innumerable polymorphisms will not be considered here, except for a few remarkable ones. Some general points must be stressed on. (a) Clinically conspicuous disorders are often the result of two alleles interacting in trans to one another. Whereas one allele causes moderate symptoms by itself, the other one is usually silent in the simple heterozygous (and exceptionally in the homozygous) state. As a result, the number of potentially pathogenic alleles is much more important than had been initially suspected. (b) The reduction or the loss of a protein within multiprotein assemblies are frequently encountered in red cell membrane genetic diseases; it leads to the disruption of the complexes with the possible disappearance of the other proteins than the mutated protein. (c) The above genes being also expressed in nonerythroid tissues, one starts finding multisyndromic conditions adding non-hematological manifestations to hemolysis. It is puzzling, though, that such situations are not more frequent. (d) In practice, the molecular diagnosis of HE and HS has reached a semi-routine stage that helps very much the paediatricians and haematologists.
红细胞的机械性能,即其抗性和弹性变形能力,归因于覆盖脂质双层的蛋白质网络以及贯穿脂质双层的蛋白质。所有蛋白质相互连接。将概述它们的结构以及相应基因的结构。众多突变使得遗传性椭圆形红细胞增多症(HE)和异形红细胞症(HP),以及最近的遗传性球形红细胞增多症(HS)被重新分类为遗传性溶血性贫血的明确亚组。HE源于分别编码血影蛋白α链和β链、蛋白4.1和血型糖蛋白C/D的SPTA1、SPTB、EL1和(极少数情况下的)GPYC基因的变化。HS源于分别编码锚蛋白、带3蛋白和蛋白4.2的ANK1、EPB3和ELB42基因以及SPTA1和SPTB基因的改变。我们将列出已知突变的清单。除了少数显著的多态性外,这里不考虑无数的多态性。必须强调一些要点。(a)临床上明显的疾病通常是两个等位基因反式相互作用的结果。一个等位基因本身会引起中度症状,而另一个等位基因在单纯杂合状态(极少数情况下在纯合状态)通常是沉默的。因此,潜在致病等位基因的数量比最初怀疑的要多得多。(b)在红细胞膜遗传病中经常会遇到多蛋白组装体中一种蛋白质的减少或缺失;这会导致复合物的破坏,除了突变蛋白外其他蛋白质可能会消失。(c)上述基因也在非红细胞组织中表达,人们开始发现多综合征情况,除了溶血外还增加了非血液学表现。然而,令人费解的是,这种情况并不更常见。(d)实际上,HE和HS的分子诊断已达到半常规阶段,这对儿科医生和血液学家有很大帮助。