High impact information on PKL/SSL2

• As GYMNOS encodes a uniformly expressed homolog of the chromatin-remodeling protein, Mi2, we argue that the unique genetic interactions do not reflect a molecular redundancy [1].
• Mutations in CRABS CLAW, the founding family member, display ectopic formation of adaxial carpel tissues only when the functions of other genes, such as GYMNOS or KANADI, are also compromised [1].
• PKL is necessary for repression of LEC1, a gene implicated as a critical activator of embryo development [2].
• Additional factors such as the CHD3 chromatin remodeling factor PICKLE (PKL) act to restrict meristematic activity in Arabidopsis leaves without repressing KNOX gene expression [3].
• In contrast, we observed that PKL is required continuously after germination to repress expression of PHERES1, a type I MADS box gene that is normally expressed during early embryogenesis in wild-type plants [4].

Biological context of PKL/SSL2

• A PKL:eGFP translational fusion is preferentially localized in the nucleus of cells, consistent with the proposed role for PKL as a chromatin remodeling factor [4].
• Thus, PKL acts at multiple points during development to regulate patterns of gene expression in Arabidopsis [4].
• In addition, genes known for their role in development, such as PICKLE/GYMNOS and PIE1, or in silencing, such as DDM1, turned out to also be involved in DNA damage response [5].

Associations of PKL/SSL2 with chemical compounds

• Taken together, our data suggest that PKL/SSL2-mediated chromatin remodeling negatively regulates auxin-mediated LR formation in Arabidopsis [6].

Regulatory relationships of PKL/SSL2

• The transcription factor ABI5 was consistently upregulated by both treatments and PKL was downregulated [7].

Analytical, diagnostic and therapeutic context of PKL/SSL2

• A candidate gene approach and microarray analysis identified nine additional genes that exhibit PKL-dependent repression of expression during germination [8].

References