Abstract
LINC complexes are evolutionarily conserved nuclear envelope bridges, composed of SUN (Sad-1/UNC-84) and KASH (Klarsicht/ANC-1/Syne/homology) domain proteins. They are crucial for nuclear positioning and nuclear shape determination, and also mediate nuclear envelope (NE) attachment of meiotic telomeres, essential for driving homolog synapsis and recombination. In mice, SUN1 and SUN2 are the only SUN domain proteins expressed during meiosis, sharing their localization with meiosis-specific KASH5. Recent studies have shown that loss of SUN1 severely interferes with meiotic processes. Absence of SUN1 provokes defective telomere attachment and causes infertility. Here, we report that meiotic telomere attachment is not entirely lost in mice deficient for SUN1, but numerous telomeres are still attached to the NE through SUN2/KASH5-LINC complexes. In Sun1−/− meiocytes attached telomeres retained the capacity to form bouquet-like clusters. Furthermore, we could detect significant numbers of late meiotic recombination events in Sun1−/− mice. Together, this indicates that even in the absence of SUN1 telomere attachment and their movement within the nuclear envelope per se can be functional.
Highlights
Nuclear anchorage and movement, including the directed repositioning of components within the nucleus, are essential for coordinated cell division, proliferation and development [1]
Though nuclear envelope (NE)-attachment of telomeres is disturbed in SUN1 deficient mice, numerous telomeres can still be found attached to the NE In recent years, it has been established by several groups that meiotic telomere attachment in mammals involves SUN1 and SUN2 as part of the NE spanning LINC complex connecting the meiotic telomeres to the cytoskeleton [11,21,22]
SUN2 compensates for the loss of SUN1 in somatic cells, SUN2 overtly does not have the competence to counterbalance loss of SUN1 in meiocytes, and it was described that telomere attachment is prevented in Sun12/2(Dex10-13) mice [11]
Summary
Nuclear anchorage and movement, including the directed repositioning of components within the nucleus, are essential for coordinated cell division, proliferation and development [1]. Peripheral, attached telomeres in SUN1 deficient oocytes and spermatocytes are seen at the ends of synaptonemal complex (SC) axes shown by SYCP3, as is the case in wildtype cells.
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