The secrets of heterochromatin

The secrets of heterochromatin
Heterochromatin is a tightly packed form of DNA that is essential for cell survival. A European backed project is investigating the molecules that control its formation and maintenance.
Associated with the formation of centromeres and telomeres, 
heterochromatin is linked with the proper segregation of genetic 
material during cell division. Heterochromatin structure is also 
implicated in gene expression. Despite its importance in cellular 
genetic control, the formation of this material is poorly understood.
The 'Study of the determinants of heterochromatin formation and 
maintenance' (HETCHROMPROJECT) project has determined key molecular 
mechanisms that control heterochromatin formation. One major player is 
ARS-binding protein 1 (ABP1). The researchers used the yeast 
Schizosaccharomyces pombe, an ideal system, as many of its genetic 
control pathways have been preserved through evolution and appear in 
mammals.
The HETCHROMPROJECT researchers found that ABP1 can repress the 
transcription of small RNAs. Other genes were identified that have a 
role to play in switching small RNA transcription on and off. 
Specifically, small RNA is derepressed in the absence of clr3 histone 
deacetylase gene and the hip3 HIRA complex gene. These two genes code 
for products that are involved in gene silencing through regulation of 
the chromatin structure.
The next phase of research before completion of the project is to 
investigate the role of novel proteins involved in heterochromatin 
regulation. In preparation for this, the scientists have set up a 
two-step genetic screen. They identified 49 deletion strains that are 
ideal for studying alterations in heterochromatin structure in the 
centromere.
Heterochromatin is important for preserving chromosome segregation 
during cell division and maintaining genomic integrity. Project research
 promises to shed light on diseases caused by changes in heterochromatin
 that impair normal gene expression.
published: 2015-01-29