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Hypothetical Model on the Functions of the WRN, BLM and MRE11
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Hypothetical Model on the Functions of the WRN, BLM and
MRE11
• WRN and BLM are genes encoding DNA helicases mutated in the human progeria
syndromes: Werner and Bloom Syndromes. MRE11 complex is mutated in genetic
instability syndromes: Nijmegen breakage syndrome and ataxia telangiectasia-like
disorder. All three may be involved in the resolution of a stalled replication fork and
in checkpoint signaling during S phase. DNA replication fork stalling results in the
formation of abnormal structures and occurs at frequencies sufficient to be a
significant source of endogenous DNA damage. BLM may be recruited to these
sites resulting in its phosphorylation by ataxia telangiectasia mutated proteinrelated protein (ATR). The activated or phosphorylated BLM determines the
proper recruitment of the MRE11 complex. WRN may be required at this point to
provide endonuclease or helicase activity. Also at this stage, WRN may be
phosphorylated by ATR or by MRE11 and NBS1, resulting in checkpoint
reinforcement. Replication recovery can also involve homologous recombination
(HR) and BRCA1 and RAD51.
Adapted from Franchitto A. et al, Human Molecular Genetics 11:2447, 2002.
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mRNP Transport through the Nuclear Pore Complex (NPC)
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Cargo Import by the Importin-Importin Pathway
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Modular Structure of Transcription Factors
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Transcription Activation by Nuclear Receptors [1 of 2]
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Transcription Activation by Nuclear Receptors [2 of 2]
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Coupled RNA Splicing and Nuclear Export
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RNA Polyadenylation
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Mammalian mRNA Polyadenylation Machinery
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RNA Maturation
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RNA-guided Epigenetic Control of Gene Expression
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Phosphorylation-driven Regulatory Switch
from Transcription Initiation to Elongation
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