The image shows a normal mitotic cell (left) compared to a cell lacking TRIM37 (right), with spindle microtubules (green), centrosomal protein centrobin (magenta) and DNA (white). Normal cells have two spindle poles that ensure proper cell division. Cells lacking TRIM37 frequently have extra spindle poles, containing a cluster of centrobin molecules, that disrupt proper cell division. Patients with Mulibrey namism lack TRIM37 and their cells show similar extra spindle poles.
TRIM37, the researchers found, is critical in preventing extra spindle poles from forming, which obstructs normal cell division, generating daughter cells with incorrect chromosomal content. But how does TRIM37 prevent the formation of extra spindle poles?
Recently published research describes how TRIM37 prevents the formation of abnormal assemblies of centrosomal proteins that can become extra spindle poles. Desai describes TRIM37 as a type of “mob breaker” that recognizes abnormal clusters of centrosomal proteins and degrades them to prevent them from forming extra spindle poles that create problems for chromosome segregation. In this manner, TRIM37 ensures accurate genome transmission during cell division.
“As loss of TRIM37 is associated with Mulibrey nanism, a tumor-prone human genetic disorder, the work also provides an explanation for what is happening at the cellular level to cause this disease,” said Desai.
Interestingly, the way TRIM37 works to prevent formation of extra spindle poles is similar to how viruses such as HIV are detected and eliminated by related TRIM proteins once they get inside cells. These findings highlight a similar molecular logic by which cells ensure accurate cell division and fight viral infections.