Dynamic interaction between TAL1 oncoprotein and LSD1 regulates TAL1 function in hematopoiesis and leukemogenesis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2012-02-06

AUTHORS

Y Li, C Deng, X Hu, B Patel, X Fu, Y Qiu, M Brand, K Zhao, S Huang

ABSTRACT

TAL1/SCL is a hematopoietic-specific oncogene and its activity is regulated by associated transcriptional co-activators and corepressors. Dysregulation of TAL1 activity has been associated with T-cell leukemogenesis. However, it remains unclear how the interactions between TAL1 and corepressors versus co-activators are properly regulated. Here, we reported that protein kinase A (PKA)-mediated phosphorylation regulates TAL1 interaction with the lysine-specific demethylase (LSD1) that removes methyl group from methylated Lys 4 on histone H3 tails. Phosphorylation of serine 172 in TAL1 specifically destabilizes the TAL1–LSD1 interaction leading to promoter H3K4 hypermethylation and activation of target genes that have been suppressed in normal and malignant hematopoiesis. Knockdown of TAL1 or LSD1 led to a derepression of the TAL1 target genes in T-cell acute lymphoblast leukemia (T-ALL) Jurkat cells, which is accompanied by elevating promoter H3K4 methylation. Similarly, treatment of PKA activator forskolin resulted in derepression of target genes by reducing its interaction with LSD1 while PKA inhibitor H89 represses them by suppressing H3K4 methylation levels. Consistent with the dual roles of TAL1 in transcription, TAL1-associated LSD1 is decreased while recruitment of hSET1 is increased at the TAL1 targets during erythroid differentiation. This process is accompanied by a dramatic increase in H3K4 methylation. Thus, our data revealed a novel interplay between PKA phosphorylation and TAL1-mediated epigenetic regulation that regulates hematopoietic transcription and differentiation programs during hematopoiesis and leukemogenesis. More... »

PAGES

5007-5018

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/onc.2012.8

DOI

http://dx.doi.org/10.1038/onc.2012.8

DIMENSIONS

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PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/22310283


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59 activation
60 activator forskolin
61 activity
62 acute lymphoblast leukemia (T-ALL) Jurkat cells
63 cell acute lymphoblast leukemia (T-ALL) Jurkat cells
64 cell leukemogenesis
65 cells
66 corepressor
67 data
68 demethylase
69 derepression
70 differentiation
71 differentiation program
72 dramatic increase
73 dual role
74 dynamic interaction
75 dysregulation
76 epigenetic regulation
77 erythroid differentiation
78 forskolin
79 function
80 genes
81 group
82 hSET1
83 hematopoiesis
84 hematopoietic transcription
85 hematopoietic-specific oncogene
86 histone H3 tail
87 hypermethylation
88 increase
89 inhibitor H89
90 interaction
91 interplay
92 kinase A
93 knockdown
94 leukemia Jurkat cells
95 leukemogenesis
96 levels
97 lymphoblast leukemia (T-ALL) Jurkat cells
98 lysine-specific demethylase
99 malignant hematopoiesis
100 methyl group
101 methylation
102 methylation levels
103 novel interplay
104 oncogene
105 oncoprotein
106 phosphorylation
107 process
108 program
109 promoter H3K4 methylation
110 protein kinase A
111 recruitment
112 recruitment of hSET1
113 regulation
114 role
115 serine 172
116 tail
117 target
118 target genes
119 transcription
120 treatment
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