Each chromosome is known to be a long DNA molecule wrapped around proteins called histones, like tiny threads on tiny spools.
“If DNA covers an area the size of a watermelon under normal conditions, then spermatozoa would only be the size of a tennis ball,” says developmental researcher Hubert Schurrle from Bonn University Hospital.
In humans and mice, two proteins called protamines replace histones to pack DNA more tightly, using every bit of space in a process called hypercondensation.
A group of researchers took a deeper look at the process of hypercondensation and looked at what happens when you take one of these protamines, PRM2.
During the entire process of spermatogenesis, a portion of the PRM2 protein, called the N-terminus, is cut off. This cutting or splitting appears to be critical to spermatogenesis.
“Proper cleavage of PRM2 appears to be critical for successful replication, however, the function of the cleaved PRM2 domain and PRM2 processing is still unknown,” the team wrote in their paper.
To find out what was going on, the researchers created mutant mice that lacked the N-terminus in PRM2 to remove them. After carefully examining the sperm, the team found that the size of PRM2 definitely needed to be reduced, as mice with unsaturated PRM2 had completely destroyed DNA.
“Removal of transition proteins during hypercondensation is bad. In addition, the condensation seems to progress very rapidly, causing DNA strand breaks,” says senior author Lina Arevalo from the University Hospital of Bonn. Not surprisingly, this rendered males infertile, but only when both copies (or alleles) of PRM2 were lost or damaged. When only one of these genes was lost, the mice were still able to reproduce.
Although we do not yet have direct evidence of this action in humans, it is possible that sometimes fertility problems in humans are caused by problems with PRM2 cleavage. The team is now investigating whether this is the case.
The search was published in PLOS Genetics.
Source: Science Alert.