High impact information on TSK

• The developmental abnormalities characteristic of bru1 mutant plants resemble those triggered by mutations in genes encoding subunits of chromatin assembly factor (CAF-1), the condensin complex, or MRE11 [1].
• BRU1, a novel link between responses to DNA damage and epigenetic gene silencing in Arabidopsis [1].
• Bru1 plants are highly sensitive to genotoxic stress and show stochastic release of transcriptional gene silencing [1].
• Comparison of bru1 with these mutants indicates cooperative roles in the replication and stabilization of chromatin structure, providing a novel link between chromatin replication, epigenetic inheritance, S-phase DNA damage checkpoints, and the regulation of meristem development [1].
• Bru1 mutations affect the stability of heterochromatin organization but do not interfere with genome-wide DNA methylation [1].

Biological context of TSK

• However, cellular localization of both TSA1-GFP and GFP-TSK changed dynamically during mitosis [2].
• In particular, both GFP-TSK and TSA1-GFP were concentrated in limited areas that are close to the ends of spindle microtubules ahead of separating chromatids [2].
• Unlike nuclear localization of TSK, the TSA1 fused with green fluorescent protein (GFP) expressed in tobacco BY-2 cells was localized in small cytoplasmic vesicles during interphase [2].
• One protein that interacts with the LGN motif of TSK in a yeast two-hybrid screen, TSK-associating protein 1 (TSA1), contains a 10-fold repeat of a unique 41 amino acid sequence [2].
• TONSOKU(TSK)/MGOUN3/BRUSHY1 from Arabidopsis thaliana, which plays an important role in the maintenance of meristem organization, contains an LGN repeat motif similar to that found in animal proteins involved in asymmetric cell division [2].

Associations of TSK with chemical compounds

• We identified a homolog of TSK from tobacco BY-2 cells (NtTSK), which showed high sequence conservation both in the LGN domain and in leucine-rich repeats with AtTSK [3].

Other interactions of TSK

• TSA1 also contains an N-terminal putative signal peptide and it interacts with the LGN motif of TSK through a C-terminal region separated from the EFE repeats by a putative membrane-spanning region [2].
• In addition, expression of SCARECROW (SCR) in the quiescent center (QC) disappeared in the disorganized RAM of tsk mutant [4].
• In the enlarged SAM of the tsk mutant, multiple centers of cells expressing WUSCHEL (WUS) were observed [4].

Analytical, diagnostic and therapeutic context of TSK

• Western blot and chromatin immunoprecipitation experiments suggested that histone H3 acetylation may be altered in the mgo3 background [5].

References