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Characterization of HAP-1 METTL9 KO cells

ABSTRACT: LAbel free quantitation of HAP1 WT and METTL9 KO cells. METTL9 is a recently established human histidine specific methyltransferase.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Leukocyte

SUBMITTER: Magnus E. Jakobsson

LAB HEAD: Magnus Jakobsson

PROVIDER: PXD023075 | Pride | 2021-04-28

REPOSITORIES: Pride

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			Action	DRS
	201019_HAP1_MT9KO_Rep01.raw	Raw
	201019_HAP1_MT9KO_Rep02.raw	Raw
	201019_HAP1_MT9KO_Rep03.raw	Raw
	201019_HAP1_MT9KO_Rep04.raw	Raw
	201019_HAP1_MT9KO_Rep05.raw	Raw

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METTL9 methylates H2B a-N-proline and suppresses human retrotransposition

Project description:The methylation of residues within histones plays a central role in regulating genome function; however, little is known about the biological importance of a-N-terminal histone methylation. Here we explored the function of the previously uncharacterized a-N methylation of mammalian histone 2B proline 1 (H2BP1me). Genome-wide analyses revealed an enrichment of H2BP1 methylation at certain transposable elements (TEs) and repetitive genomic sequences. We identified a novel histone methyltransferase, METTL9, which specifically methylates H2BP1. Depletion of METTL9 led to reduced H2BP1me2 levels, an accumulation of gH2A.X, expression activation of some TEs, and increased retrotransposition of a human LINE-1 containing a reporter gene; the latter being a unique feature amongst histone modifiers described to date. These data suggest that reduced H2BP1 methylation may lead to increased TE activity and genome instability. Indeed, decreased levels of H2BP1 methylation in colon tumors correlated with an increase in LINE-1 protein expression. Furthermore, METTL9 depletion in cultured cells led to an enhancement of cellular proliferation, invasion, and migration, suggesting that a loss of H2BP1 methylation could play a role in cancer progression. Thus, we have identified a new role for H2BP1 N-terminal histone methylation in regulating chromatin function and perhaps disease progression, thereby highlighting the role of METTL9 as a novel guardian of genomic stability.

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Characterization of METTL9-mediated methylation of DNAJB12

Project description:The analysis is part of a study aimed at characterizing a new human histidine-specific methyltransferase denoted METTL9. The putative METTL9 substrate DNAJB12 was immunoprecipitated from HEK293 cells and its PTM status was assessed by LC-MSMS.

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METTL9 sustains vertebrate neural development primarily via non-catalytic functions

Project description:METTL9 is an enzyme catalysing histidine N1-methylation (1-MH). Given the high levels of this methyltransferase during vertebrate nervous system development, we dissected the roles of Mettl9 during this relevant physiological process. We generated three mouse embryonic stem cell lines featuring a complete Mettl9 knock-out, an inducible degron system, and the endogenous expression of a catalytically inactive protein. Additionally, we employed Xenopus laevis to down-regulate Mettl9 during neural development in vivo. Our multi-omic data indicate that METTL9 exerts a conserved role in sustaining vertebrate neurogenesis. Surprisingly, both perturbation of METTL9 catalytic activity and depletion of METTL9 protein levels without affecting global 1-MH levels show milder neural commitment defects, suggesting a role for both METTL9 catalytic and non-enzymatic activities. These converge towards the secretory pathway, where METTL9 co-localises with the Golgi apparatus and interacts with key regulators of cellular transport, endocytosis and Golgi integrity.

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Project description:Exploring the interactome of the human putative methyltransferase enzyme METTL9.

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The methyltransferase METTL9 mediates pervasive 1-methylhistidine modification in mammalian proteomes

Project description:Post-translational methylation plays a crucial role in regulating and optimizing protein function. Protein histidine methylation, occurring as the two isomers 1- and 3- methylhistidine (1MH and 3MH), was first reported five decades ago, but remains largely unexplored. Here we report that METTL9 is a broad-specificity methyltransferase (MTase) that mediates the formation of the majority of 1MH present in mouse and human proteomes. The minimal requirement for METTL9-catalyzed methylation is a His-x-His (HxH) motif, where "x" is preferably a small amino acid, allowing METTL9 to methylate a number of HxH-containing proteins. Here, we show that the immunomodulatory protein S100A9 and the NDUFB3 subunit of mitochondrial respiratory Complex I are methylated at HxH motif using MALDI-TOF MS.

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Molecular basis for METTL9-mediated N1-histidine methylation.

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METTL9-SLC7A11 axis promotes hepatocellular carcinoma progression through ferroptosis inhibition.

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