In order to clarify the relationship between meiotic pairing and progress of spermatogenesis, an analysis of male meiotic pairing was carried out in four reciprocal translocation heterozygotes and two double heterozygotes for two semi-identical reciprocal translocations. The reciprocal translocations were chosen to range from fertility (T70H/+) through almost complete sterility (T31H/+) to complete sterility (T32H/+, T42/H+). If meiotic pairing in the translocation multivalent was incomplete, it concerned terminal or probably more often proximal chromosome segments (Chain IV). If both segments failed to pair the multivalent symbol is Chain III + I. Complete pairing is symbolized by Ring IV. To contrast and complement observations of this type, the double heterozygotes were introduced. Males of this type in theory possess two heteromorphic bivalents with a central area of incomplete meiotic pairing (loop formation). Of the T70H/T1Wa double heterozygotes, 36% of the males are capable of inducing at least one decidual reaction in two females whereas for T26H/T2Wa, 79% of the males can do so. For the reciprocal translocations, it was found that proximity of the multivalent to the sex bivalent during pachytene increased in the order Ring IV, Chain IV, Chain III + I. The degree of spermatogenic impairment as measured from cell counts in histological sections and tubular whole mounts, is positively related to the frequency of proximity between the sex chromosomes and the translocation multivalent and thus to lack of meiotic pairing within the multivalent. The meiotic pairing analysis of the double heterozygotes yielded the following findings. For the long heteromorphic bivalents a true loop was never seen in T70H/T1Wa and only rarely observed in T26H/T2Wa. Small marker bivalents of both types were usually recognizable by the following criteria: pairing confined to distal or proximal segments, both distal and proximal segments pairing and loop formation and pairing covering the entire length of both "homologues" but the longer one often with a "thickened" lateral element. The same positive correlation between the absence of pairing (proximal, distal or central) and the proximity of the small marker bivalent synaptonemal complex to the sex bivalent has been found as for unpaired segments within reciprocal translocation multivalents. One unexpected finding was the occurrence of diploid spermatids and spermatozoa especially in T32H/+ males (70-91%) but also in T31H/+ (3-39%).

Tertiary trisomic males, carrying the small translocation chromosome from the T(1;13)7OH reciprocal mouse translocation as the extra chromosome, are oligospermic. Uterine and oviductal sperm counts were congruent to 10% of normal. Of the uterine spermatozoa, 77-2% were morphologically abnormal compared with 24-6% in the oviduct. Oligospermy in the tertiary trisomic males leads to delayed fertilization; 34-8% of the 109 eggs scored between 5-5--9-5 hr after mating were fertilized compared with 52-1% (n=343) at Day 2. Of the 179 morulae/blastocysts recovered at Day 4, 46-9% contained the small marker chromosome, which agrees with earlier cytological studies on secondary spermatocytes. These results indicate that euploid and aneuploid spermatozoa are formed in about equal numbers and there is no relationship between sperm morphology and karyotype.

Female mice of two age groups, 3–4 and 11–14 months old, homozygous for the T(1;13)70H reciprocal mouse translocation were used for cytological observations of bivalents (in primary oocytes) and metaphase II chromosomes (in secondary oocytes). Special attention was given to the behavior of the long (13¹) and short (1¹³) marker chromosomes. In primary oocytes, univalents were considered “true” or “opposite.” The aged females showed an eight-fold increase in “true” univalent frequency for chromosome 1¹³ over the young ones. A nine-fold rise for nondisjunction with regard to this chromosome was observed. For the other chromosomes, these factors were 2 and 1.7, respectively. The absolute levels of nondisjunction remained low at old age (1.42% for chromosome 1¹³, 1.22% for all other chromosomes). The long marker bivalent 13¹ was used for chiasma counts. No change in chiasma number with age was observed. It is argued that poorer physiological conditions within the maturing oocytes of older females are the major cause for both the increasing frequencies of “true” and “opposite” univalents and the increased incidence of nondisjunction.

Summary. Pig embryos (3\p=n-\4days old) were

A dose of 7 IU human chorionic gonadotropin (hCG) given 14 h before the expected LH peak on proestrus significantly increased embryonic mortality in Swiss random-bred female mice to 5 5% of the number of corpora lutea. The use of luteinizing hormone-releasing hormone in a similar injection protocol did not induce embryonic death. The effect found in Swiss random-bred mice resembles that of a dose of 20 IU hCG in the rat. Afternoon-day-4 mouse embryos contained 39.1 ± 12.6 nuclei after hCG-induced ovulation compared to 46.2 ± 16.6 nuclei after spontaneous ovulation. For early-day-5 embryos of the rat, these figures were 34.2 ± 10.1 and 31.7 ± 8.4, respectively (mating was early on day 1). Numerical chromosome errors were estimated in secondary oocytes of the mouse and early-day-5 embryos of the rat. Compared with data from the literature, hCG seems to induce some extra meiotic nondisjunction in the rat only. Combining all genetic and physiological data, the loss of fecundity after hCG-induced ovulation is a maternal effect.