MEIS homeodomain proteins facilitate PARP1/ARTD1-mediated eviction of histone H1

Hau, Ann-Christin; Grebbin, Britta Moyo; Agoston, Zsuzsa; Anders-Maurer, Marie; Müller, Tanja; Groß, Anja; Kolb, Jasmin; Langer, Julian D.; Döring, Claudia; Schulte, Dorothea

doi:10.1083/jcb.201701154

Cited by 26 publications

(44 citation statements)

References 53 publications

(103 reference statements)

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“…Once differentiation is induced, MEIS associates with chromatin-bound PBX1, it recruits poly-ADP-ribose polymerase 1 (PARP1) and then initiates PARP1-mediated eviction of H1 from chromatin. These findings delineate a sequence of events by which a PBX/MEIS complex facilitates chromatin accessibility of transcriptionally inactive genes in neural progenitor cells (Hau et al 2017). Overall, it has been reported that PBX1 primes genes for activation in different systems and can bind to its target sites when chromatin is still compacted.…”

Section: Partnerships Of Pbc Tfsmentioning

confidence: 57%

‘Building a perfect body’: control of vertebrate organogenesis by PBX-dependent regulatory networks

2019

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Pbx genes encode transcription factors that belong to the TALE (three-amino-acid loop extension) superclass of homeodomain proteins. We have witnessed a surge in information about the roles of this gene family as leading actors in the transcriptional control of development. PBX proteins represent a clear example of how transcription factors can regulate developmental processes by combinatorial properties, acting within multimeric complexes to implement activation or repression of transcription depending on their interaction partners. Here, we revisit long-emphasized functions of PBX transcription factors as cofactors for HOX proteins, major architects of the body plan. We further discuss new knowledge on roles of PBX proteins in different developmental contexts as upstream regulators of Hox genes-as factors that interact with non-HOX proteins and can work independently of HOX-as well as potential pioneer factors. Committed to building a perfect body, PBX proteins govern regulatory networks that direct essential morphogenetic processes and organogenesis in vertebrate development. Perturbations of PBX-dependent networks can cause human congenital disease and cancer.

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Section: Partnerships Of Pbc Tfsmentioning

confidence: 57%

‘Building a perfect body’: control of vertebrate organogenesis by PBX-dependent regulatory networks

2019

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“…Surprisingly, we observed the expression of neurogenic fate determinants already in the NSC (Beckervordersandforth et al , and Table EV1). The qPCR validation of these data showed that neurogenic fate determinants such as MEIS2 (Agoston et al , ; Hau et al , ), SOX11 (Mu et al , ), or PAX6 (Ninkovic et al , ) were already expressed in both activated, EGFR‐positive NSCs (aNSCs) and quiescent, EGFR‐negative NSCs (qNSCs), but virtually absent in diencephalic astrocytes (Figs A and EV1A). The expression levels of these neurogenic fate determinants further increased in the prospectively isolated progeny of NSCs, such as neuroblasts (Figs A and EV1A, and Table EV1; see Beckervordersandforth et al , ; Codega et al , ; Fischer et al , , for the sorting procedure).…”

Section: Resultsmentioning

confidence: 88%

“…To examine how this transcriptional regulation is reflected at the protein level in qNSCs, we used immunohistochemistry (IHC) for two factors following the above described expression pattern: MCM6, a transcription factor regulating proliferation (Noseda & Karsan, ), and MEIS2, regulating neurogenesis in the SEZ (Agoston et al , ; Hau et al , ). We used a long‐term BrdU label‐retaining protocol (Codega et al , ) allowing detection of a subset NSCs and their progeny.…”

Section: Resultsmentioning

confidence: 99%

Choroid plexus‐derived miR‐204 regulates the number of quiescent neural stem cells in the adult brain

et al. 2019

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Regulation of adult neural stem cell (NSC) number is critical for lifelong neurogenesis. Here, we identified a post-transcriptional control mechanism, centered around the microRNA 204 (miR-204), to control the maintenance of quiescent (q)NSCs. miR-204 regulates a spectrum of transcripts involved in cell cycle regulation, neuronal migration, and differentiation in qNSCs. Importantly, inhibition of miR-204 function reduced the number of qNSCs in the subependymal zone (SEZ) by inducing pre-mature activation and differentiation of NSCs without changing their neurogenic potential. Strikingly, we identified the choroid plexus of the mouse lateral ventricle as the major source of miR-204 that is released into the cerebrospinal fluid to control number of NSCs within the SEZ. Taken together, our results describe a novel mechanism to maintain adult somatic stem cells by a niche-specific miRNA repressing activation and differentiation of stem cells.

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“…In fact, differential MEIS binding in a specific BAs is generally a very good predictor for matching changes in enhancer activity in the same tissue. Based on our observations and the well-established role of MEIS in transcriptional activation (Choe et al, 2009; Hau et al, 2017; Hyman-Walsh et al, 2010), we propose a model of transcriptional activation, where TALE (MEIS) TFs function as a broad or general activators and HOX paralog selectivity is mainly directed at harnessing TALE functional activity at selected locations. Using their recognition motifs, HOX and/or tissue-specific TFs select specific MEIS binding locations, where they stabilize MEIS binding to generate precise functional outputs, or patterns of enhancer activation (Fig.…”

Section: Discussionmentioning

confidence: 83%

“…7). Interestingly, MEIS2 interacts with PARP1 (Hau et al, 2017), a large enzyme capable of triggering phase condensation (Altmeyer et al, 2015). Increasing MEIS residence time (as a result of the cooperation with HOX and other TFs) may favour PARP1 recruitment at selected loci and, in turn, generate the liquid-liquid phase transitions observed to promote gene activation (Boija et al, 2018; Hnisz et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

HOX paralogs selectively convert binding of ubiquitous transcription factors into tissue-specific patterns of enhancer activation

Bridoux

Zarrineh

Mallen

et al. 2019

Preprint

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19Gene expression programs determine cell fate in embryonic development and their 20 dysregulation results in disease. Transcription factors (TFs) control gene expression by 21 binding to enhancers, but how TFs select and activate their target enhancers is still unclear. 22HOX TFs share conserved homeodomains with highly similar sequence recognition 23properties, yet they impart the identity of different animal body parts. To understand how 24 HOX TFs control their specific transcriptional programs in vivo, we compared HOXA2 and 25 HOXA3 binding profiles in the mouse embryo. HOXA2 and HOXA3 directly cooperate with 26 TALE TFs and selectively target different subsets of a broad TALE chromatin platform. 27Binding of HOX and tissue-specific TFs convert low affinity TALE binding into high 28 confidence, tissue-specific binding events, which bear the mark of active enhancers. We 29 propose that HOX paralogs, alone and in combination with tissue-specific TFs, generate 30 tissue-specific transcriptional outputs by modulating the activity of TALE TFs at selected 31 enhancers. 32 33 Introduction 34 Gene expression programs instruct and maintain cell fate in embryonic development and 35 adult tissue homeostasis. Transcription factors (TFs) control gene expression by binding to 36 enhancers (Reiter et al., 2017; Spitz and Furlong, 2012). However, we still have no clear 37 idea of how TFs select their precise sets of target enhancers. While TFs contain DNA 38 binding domains which recognize DNA in a sequence-specific manner, these interactions 39 are typically insufficient to direct a TF to its functional targets. 40Transcriptional regulation is mediated by TFs working together, rather than in isolation. The 41 widespread occurrence of collaborative TF binding is imposed by chromatin. A single TF 42 cannot easily compete with nucleosomes to access DNA, but multiple TFs that recognize 43 closely spaced binding sites can effectively displace nucleosomes and indirectly facilitate 44 each other's binding (Mirny, 2010; Moyle-Heyrman et al., 2011). Such indirect cooperativity 45 can also result in TFs recognizing low affinity sites, i.e. sites that deviate from their optimal 46 3 consensus in vitro (Farley et al., 2015). Recent observations indicate that TF cooperativity 47 does not end at binding enhancers: clusters of enhancer-bound TFs concentrate co-48 activators and other nuclear factors via dynamic fuzzy interactions, driven by their 49 intrinsically disordered regions (IDRs). IDRs function in molecular recognition and mediate 50 the interaction with a diversity of regulatory proteins (Cumberworth et al., 2013; Staby et al., 51 2017) to promote the liquid-liquid phase transition associated with gene activation (Boija et 52 al., 2018). Thus, the formation, on DNA segments, of regulatory complexes made of different 53 combinations of factors, is key to activation of gene expression. These distinct combinations 54 of TFs produce virtually inexhaustible flavours of gene expression and cell fate (Spitz and 55 Furlong, 2012).56...

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MEIS homeodomain proteins facilitate PARP1/ARTD1-mediated eviction of histone H1

Cited by 26 publications

References 53 publications

‘Building a perfect body’: control of vertebrate organogenesis by PBX-dependent regulatory networks

‘Building a perfect body’: control of vertebrate organogenesis by PBX-dependent regulatory networks

Choroid plexus‐derived miR‐204 regulates the number of quiescent neural stem cells in the adult brain

HOX paralogs selectively convert binding of ubiquitous transcription factors into tissue-specific patterns of enhancer activation

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