Hum Genet (1991) 88 : 124 9 Springer-Verlag1991 Letter to the editors C-anaphase versus premature centromere division H. Rivera and M. G. Dominguez Divisi6n de Genrtica, Instituto Mexicano del Seguro Social, Ap. Postal 1-3838, Guadalajara, Jalisco, Mexico Received December 17, 1990 / Revised March 1, 1991 A review of the current literature reveals that the term premature centromere division (PCD) is often used to designate certain mitotic configurations which are also referred to as C-anaphases (cf. Chamla 1988). Such a confusion results from the split aspect of the centromeric regions in both conditions and disregard for their distinc- tive features. It should be stressed that the appearance and function of the centromeric region sharply discrimi- nates between the two phenomena. In a C-anaphase the centromeric regions of all, or most, chromosomes, even if split, still show the primary constriction and are Cd- band positive (Chamla et al. 1980; Madan et al. 1987); in contrast, a chromosome with PCD takes on an acentric aspect and is Cd-band-negative (Fitzgerald et al. 1975; Nakagome et al. 1984), the other chromosomes being normal. Consequently, sister chromatids are splayed in C-anaphases and parallel in PCD chromosomes (Chamla 1988). Furthermore, C-anaphases seem to be harmless, age-independent and inherited as an autosomal domi- nant trait (Chamla 1988; McKusick 1990), whereas PCD predisposes to nondisjunction, is age-dependent and does not show a clear pattern of inheritance (Fitzgerald et al. 1975; Galloway and Buckton 1978; McKusick 1990). Regarding nomenclature we agree with Therman (1986) in considering the denomination PCD to be mis- leading, since the underlying mechanism is centromere inactivation. The term C-anaphase is also inadequate, because similar configurations can be seen in cultures without colchicine (Rudd et al. 1983; Gabarron et al. 1986; Madan et al. 1987) and because the ratio of C- anaphases remained unchanged despite a 200-fold in- crease in the concentration of the cytotoxic agent (Cham- Offprint requests to: H. Rivera la et al. 1980). Nevertheless, rather than substitute more precise terms for these unsatisfactory ones, we consider that they should be used unambiguously and only to con- vey the original connotations. References Chamla Y (1988) C-anaphases in lymphocyte cultures versus pre- mature centromere division syndromes. Hum Genet 78:111- 114 Chamla Y, Roumy M, Lassrgues M, Battin J (1980) Altered sen- sitivity to colchicine and PHA in human cultured cells. Hum Genet 53: 249-253 Fitzgerald PH, Pickering AF, Mercer YM, Meithke PM (1975) Pre- mature centromere division: a mechanism of non-disjunction causing X chromosome aneuploidy in somatic cells of man. Ann Hum Genet 38: 417-428 Gabarron J, Jimrnez A, Glover G (1986) Premature centromere division dominantly inherited in a subfertile family. Cytogenet Cell Genet 43 : 69-71 Galloway SM, Buckton K (1978) Aneuploidy and ageing: chromo- some studies on a random sample of the population using G- banding. Cytogenet Celt Genet 20: 78-95 Madan K, Lindhout D, Palan A (1987) Premature centromere di- vision (PCD): a dominantly inherited anomaly. Hum Genet 77 : 193-196 McKusick VA (1990) Mendelian inheritance in man, 9th edn. Johns Hopkins University Press, Baltimore London Nakagome Y, Abe T, Misawa S, Takeshita T, Iinuma K (1984) The "loss" of centromeres from chromosomes of aged women. Am J Hum Genet 36: 398-404 Rudd NL, Teshima IE, Martin RH, Sisken JE, Weksberg R (1983) A dominantly inherited cytogenetic anomaly: a possible cell di- vision mutant. Hum Genet 65 : 117-121 Therman E (1986) Human chromosomes, 2nd edn. Springer, Ber- lin Heidelberg New York