Lateral element

Abstract: Completion of meiosis in mammals depends on the formation of the synaptonemal complex, a tripartite structure that physically links homologous chromosomes during prophase I. Several components of the synaptonemal complex are known, including constituents of the cohesin core, the axial/lateral element and the transverse filaments. No protein has previously been identified as an exclusive component of the central element. Mutations in some synaptonemal-complex proteins results in impaired meiosis. In humans, cases of male infertility have been associated with failure to build the synaptonemal complex. To search for new components of the meiotic machinery, we have used data from microarray expression profiling and found two proteins localising solely to the central element of the mammalian synaptonemal complex. These new proteins, SYCE1 and CESC1, interact with the transverse filament protein SYCP1, and their localisation to the central element appears to depend on recruitment by SYCP1. This suggests a role for SYCE1 and CESC1 in synaptonemal-complex assembly, and perhaps also stability and recombination.

Abstract: In vitro, the human Rad51 protein (hRad51) promotes homologous pairing and strand exchange reactions suggestive of a key role in genetic recombination. To analyse its role in this process, polyclonal antibodies raised against hRad51 were used to study the distribution of Rad51 in human and mouse spermatocytes during meiosis I. In human spermatocytes, hRad51 was found to form discrete nuclear foci from early zygotene to late pachytene. The foci always co-localized with lateral element proteins, components of the synaptonemal complex (SC). During zygotene, the largest foci were present in regions undergoing synapsis, suggesting that Rad51 is a component of early recombination nodules. Pachytene nuclei showed a greatly reduced level of Rad51 labelling, with the exceptions of any asynapsed autosomes and XY segments, which were intensely labelled. The distribution of Rad51 in mouse spermatocytes was similar to that found in human spermatocytes, except that in this case Rad51 was detectable at leptotene. From these results, we conclude that the Rad51 protein has a role in the interhomologue interactions that occur during meiotic recombination. These interactions are spatially and temporally associated with synapsis during meiotic prophase I.

Abstract: Surface spread spermatocytes of mice heterozygous for a tandem duplication show nuclei in late zygotene-early pachytene in which the heteromorphic synaptonemal complex (SC) contains a lateral element that is buckled out into an unpaired loop as a consequence of the added length of the duplication (estimated in another study to be 21.7%, with breakpoints at 0.50 and 0.72 of the length of the chromosome). The ends of the buckle, marking the interstitial termini of synapsis proceeding from opposite directions, vary over a wide range of positions, but within limits: the proximal end of the loop does not exceed the distal end of the duplication segment, while the distal end of the loop does not lie closer to the kinetochore than the proximal end of the segment. Thus, synapsis (SC formation) at zygotene is restricted to homologous regions (exclusive homosynapsis). — In the last half of pachytene, no buckles are found, only simple SCs with lateral elements of equal length, as a consequence of synaptic adjustment. Intermediate stages of adjustment are found throughout the first half of pachytene. Shortly after homosynapsis is complete, synaptic adjustment begins: the ends of the duplication loop separate (desynapsis of homosynapsed regions); the long axis shortens with respect to the short axis in both the unpaired loop and in the SC portions; asymmetrical twists take up inequalities; the loop is reduced to from 1 to 3 asymmetrical twists; the axes (lateral elements) equalize as the long axis shortens; and a simple SC is formed, indistinguishable from others in the complement, in which the region of the duplication and those adjacent to it have heterosynapsed, while the distal regions of the SC are presumably still homosynapsed. Synaptic adjustment evidently involves two sequential events: localized instability of the homosynapsed condition, leading to desynapsis, then restoration of the SC by heterosynapsis. Adjustment therefore represents the loss of strict homosynapsis. It is concluded that the asymmetry produced by the duplication loop constitutes an instability that triggers synaptic adjustment.