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Tài liệu Báo cáo khoa học: Golgi reassembly stacking protein 55 interacts with membrane-type (MT) 1-matrix metalloprotease (MMP) and furin and plays a role in the activation of the MT1-MMP zymogen pdf

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Tiêu đề Golgi reassembly stacking protein 55 interacts with membrane-type (MT) 1-matrix metalloprotease (MMP) and furin and plays a role in the activation of the MT1-MMP zymogen
Tác giả Christian Roghi, Louise Jones, Matthew Gratian, William R. English, Gillian Murphy
Trường học University of Cambridge
Chuyên ngành Molecular biology
Thể loại Journal article
Năm xuất bản 2010
Thành phố Cambridge
Định dạng
Số trang 18
Dung lượng 878,77 KB

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Further analysis revealed that GRASP55 associated with the cytoplasmic domain of both proteases and that the LLY573motif in the MT1-MMP intracellular domain was crucial for the interacti

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membrane-type (MT) 1-matrix metalloprotease (MMP) and furin and plays a role in the activation of the MT1-MMP zymogen

Christian Roghi1,2, Louise Jones2*, Matthew Gratian2, William R English1,2and Gillian Murphy1,2

1 Cancer Research UK Cambridge Research Institute, The Li Ka Shing Centre, UK

2 Cambridge Institute for Medical Research, UK

Keywords

furin; GRASP55; intracellular traffic;

MT1-MMP; protease

Correspondence

C Roghi, Cancer Research UK Cambridge

Research Institute, The Li Ka Shing Centre,

Robinson Way, Cambridge CB2 0RE, UK

Fax: +44 (0)1223 404573

Tel: +44 (0)1223 404472

E-mail: chr26@cam.ac.uk

*Present address

KuDOS Pharmaceuticals Ltd, Cambridge

Science Park, UK

(Received 25 March 2010, revised 14 May

2010, accepted 28 May 2010)

doi:10.1111/j.1742-4658.2010.07723.x

Membrane-type 1 matrix metalloproteinase (MT1-MMP) is a proteinase involved in the remodelling of extracellular matrix and the cleavage of a number of substrates MT1-MMP is synthesized as a zymogen that requires intracellular post-translational cleavage to gain biological activity Furin,

a member of the pro-protein convertase family, has been implicated in the proteolytic removal of the MT1-MMP prodomain sequence In the present study, we demonstrate a role for the peripheral Golgi matrix protein GRASP55 in the furin-dependent activation of MT1-MMP MT1-MMP and furin were found to co-localize with Golgi reassembly stacking protein

55 (GRASP55) Further analysis revealed that GRASP55 associated with the cytoplasmic domain of both proteases and that the LLY573motif in the MT1-MMP intracellular domain was crucial for the interaction with GRASP55 Overexpression of GRASP55 was found to enhance the forma-tion of a complex between MT1-MMP and furin Finally, we report that disruption of the interaction between GRASP55 and furin led to a reduc-tion in pro-MT1-MMP activareduc-tion Taken together, these data suggest that GRASP55 may function as an adaptor protein coupling MT1-MMP with furin, thus leading to the activation of the zymogen

Structured digital abstract

l MINT-7897990 : Furin (uniprotkb: P09958 ) and GRASP55 (uniprotkb: Q9H8Y8 ) colocalize ( MI:0403 ) by fluorescence microscopy ( MI:0416 )

l MINT-7897801 : GRASP55 (uniprotkb: Q9R064 ) physically interacts ( MI:0915 ) with MT2-MMP (uniprotkb: P51511 ) by two hybrid ( MI:0018 )

l MINT-7897821 : GRASP55 (uniprotkb: Q9R064 ) physically interacts ( MI:0915 ) with MT3-MMP (uniprotkb: P51512 ) by two hybrid ( MI:0018 )

l MINT-7897577 : GRASP55 (uniprotkb: Q9R064 ) and MT1-MMP (uniprotkb: P50281 ) coloca-lize ( MI:0403 ) by fluorescence microscopy ( MI:0416 )

l MINT-7897366 : MT1-MMP (uniprotkb: P50281 ) physically interacts ( MI:0915 ) with GRASP55 (uniprotkb: Q9H8Y8 ) by anti bait coimmunoprecipitation ( MI:0006 )

Abbreviations

ECM, extracellular matrix; EGFP, enhanced green fluorescent protein; EYFP, enhanced yellow fluorescent protein; FACS, fluorescence-activated cell sorting; GFP, green fluorescent protein; GRASP, Golgi reassembly stacking protein; GRASP55F, FLAG-tagged GRASP55;

IB, immunoblotting; ICD, intracellular domain; M2H, mammalian two-hybrid; MMP, matrix metalloprotease; MT1/EYFP, EYFP-tagged MT1-MMP; MT1/MYC, Myc-tagged MT1-MMP; MT-MMP, membrane-type MMP; PDZ, PSD-95/SAP90 Drosophila septate junction protein discs-large and epithelial tight junction ZO-1; TGF, transforming growth factor; TGN, trans-Golgi network.

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Extracellular matrix (ECM) remodelling is a crucial

process occurring during cell migration and invasion

in various physiological (i.e embryonic development,

ovulation, angiogenesis, wound healing) and

patho-logical processes, including rheumatoid arthritis,

tumour growth, invasion and metastasis [1] Of all

the different proteolytic systems involved in ECM

turnover, the matrix metalloproteinases (MMPs) have

been reported to exert a dominant effect [2] MMPs

are a large family of structurally and functionally

related multi-domain zinc-dependent endopeptidases

that collectively are able to degrade virtually all

pro-teins of the ECM MMPs are mainly soluble

enzymes released by the cell in the extracellular

milieu, although membrane-bound MMPs (membrane

type-MMPs or MT-MMPs) have also been identified

and are ideally positioned for regulating pericellular

proteolysis [3]

Membrane-type 1 matrix metalloproteinase

(MT1-MMP; MMP14; EC 3.4.24.80) is by far the most

extensively studied member of the MT-MMP

sub-family MT1-MMP is a type 1 transmembrane MMP

involved in pericellular ECM turnover [4], as well as in

the proteolytic processing of cell surface receptors

[4,5] MT1-MMP is also involved in the activation of

pro-MMP2 and pro-MMP13, leading to the indirect increase in its repertoire of substrates [6,7]

MT1-MMP has a wide spectrum of cellular func-tions [5,8] Elevated MT1-MMP expression, which is well documented in many tumours, has been correlated with key processes of tumour progression [9,10], including angiogenesis [11], cell migration and invasion [12], cell growth [13], and metastatic spread Inhibition

or silencing of the protease has been found to significantly reduce the invasive phenotype of tumour cells, implicating a leading role for MT1-MMP in such processes [12,14]

There is mounting evidence that the short intracellu-lar domain (ICD) of MT1-MMP (21 amino acids) plays an important role in multiple MT1-MMP-medi-ated cellular events [15] MT1-MMP ICD has been involved in cell migration [16] and invasion into recon-stituted basement membrane [17,18] The MT1-MMP ICD is also critical for the intracellular trafficking of the enzyme [19–23] and its targeting to invadopodia in invasive cells [24] The ICD of MT1-MMP has been found to modulate multiple signal transduction path-ways [16,25–27] and participates in the homophilic interaction between MT1-MMP monomers [28] Recently, the LL572 di-leucine motif has been reported

l MINT-7897617 , MINT-7897659 , MINT-7897681 , MINT-7897702 , MINT-7897725 ,

MINT-7898032 , MINT-7898011 , MINT-7897907 , MINT-7897884 : GRASP55 (uniprotkb: Q9R064 ) physically interacts ( MI:0915 ) with MT1-MMP (uniprotkb: P50281 ) by two hybrid ( MI:0018 )

l MINT-7898002 : MT1-MMP (uniprotkb: P50281 ) physically interacts ( MI:0914 ) with Furin (uniprotkb: P09958 ) by anti bait coimmunoprecipitation ( MI:0006 )

l MINT-7897500 : MT1-MMP (uniprotkb: P50281 ) and Giantin (uniprotkb: Q14789 ) colocalize ( MI:0403 ) by fluorescence microscopy ( MI:0416 )

l MINT-7897750 , MINT-7897394 : GRASP55 (uniprotkb: Q9R064 ) physically interacts ( MI:0915 ) with MT1-MMP (uniprotkb: P50281 ) by anti tag coimmunoprecipitation ( MI:0007 )

l MINT-7897562 : MT1-MMP (uniprotkb: P50281 ) and GRASP55 (uniprotkb: Q9H8Y8 ) coloca-lize ( MI:0403 ) by fluorescence microscopy ( MI:0416 )

l MINT-7897512 : TGN46 (uniprotkb: O43493 ) and MT1-MMP (uniprotkb: P50281 ) colocalize ( MI:0403 ) by fluorescence microscopy ( MI:0416 )

l MINT-7897921 , MINT-7897975 : GRASP55 (uniprotkb: Q9R064 ) physically interacts ( MI:0915 ) with Furin (uniprotkb: P09958 ) by two hybrid ( MI:0018 )

l MINT-7898052 , MINT-7897410 : MT1-MMP (uniprotkb: P50281 ) physically interacts ( MI:0915 ) with GRASP55 (uniprotkb: Q9R064 ) by anti bait coimmunoprecipitation ( MI:0006 )

l MINT-7897951 : GRASP55 (uniprotkb: Q9R064 ) physically interacts ( MI:0915 ) with PC7 (uniprotkb: Q16549 ) by two hybrid ( MI:0018 )

l MINT-7897866 : GRASP55 (uniprotkb: Q9R064 ) physically interacts ( MI:0915 ) with MT5-MMP (uniprotkb: Q9Y5R2 ) by two hybrid ( MI:0018 )

l MINT-7897633 : GRASP55 (uniprotkb: Q9R064 ) physically interacts ( MI:0915 ) with TGFA (uniprotkb: P01135 ) by two hybrid ( MI:0018 )

l MINT-7897551 : GRASP55 (uniprotkb: Q9H8Y8 ) and Giantin (uniprotkb: Q14789 ) colocalize ( MI:0403 ) by fluorescence microscopy ( MI:0416 )

l MINT-7897938 : GRASP55 (uniprotkb: Q9R064 ) physically interacts ( MI:0915 ) with PC5/6B (uniprotkb: Q04592 ) by two hybrid ( MI:0018 )

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to influence the O-glycosylation pattern of MT1-MMP

[29] Post-translational modifications of the

MT1-MMP ICD have also been reported with the

palmitoy-lation of the cysteine 574 (C574) residue [30] and the

phosphorylation of the tyrosine 573 (Y573) [31] and

threonine 567 (T567) [32] residues The MT1-MMP

ICD has been reported to interact with the

multifunc-tional protein p32/gC1qR [21], a protein with

homol-ogy to members of the Cupin superfamily (MTCBP-1)

[33], as well as with the l2 subunit of the

clathrin-coated pits adapter protein 2 (AP-2) [18] and

phospho-caveolin-1 in src overexpressing cells [34]

Golgi reassembly stacking protein 55 (GRASP55) is

a peripheral Golgi matrix protein that has been

impli-cated, in vitro, in the post-mitotic stacking of Golgi

cis-ternae [35] Cryo-electron microscopy has shown that

GRASP55 is found predominantly in the

medial-cister-nae of the Golgi complex of HeLa cells [35]

GRASP55 interacts with Golgin-45 and the complex is

crucial for maintaining Golgi structure [36] In

addi-tion to its contribuaddi-tion to the Golgi exoskeleton,

GRASP55 has also been reported to be involved in the

intracellular transport of pro-transforming growth

fac-tor (TGF)-a [37], CD8a or the frizzled recepfac-tor Fz4

[38], as well as in the Golgi retention of p24a, a

mem-ber of the p24 family of cargo receptors [39]

In the present study, we report in detail on the

inter-action between the MT1-MMP ICD and GRASP55

using a mammalian two-hybrid (M2H) system Using

this approach, we have identified the GRASP55

bind-ing site in the ICD of MT1-MMP, as well as the

GRASP55 domains involved in the interaction with

MT1-MMP ICD We also describe the GRASP55

interaction with the furin ICD, and provide evidence

that GRASP55 could play an important role in the

furin-mediated proteolytic activation of the

MT1-MMP zymogen

Results

MT1-MMP co-immunoprecipitates with GRASP55

Although the presence of MT1-MMP and GRASP55

(p59) in the same complex has been suggested by Kuo

et al [37], the functional implications of this

interac-tion have yet to be fully investigated In steady-state

HT1080 cells, MT1-MMP is mainly present at the cell

surface and in the endosomal compartment [22] and

virtually no protease can be detected in the Golgi

apparatus We therefore transfected these cells with an

exogenous wild-type MT1-MMP cDNA (Fig 1A),

aiming to detect the protease in the early secretory

pathway Cells were then lysed and the extract was

A

60 50 40

IB: MT1-MMP

MT1-MMP pCDNA3.1 Zeo+

kDa

+ – – +

+ – – +

60 50 40

IB: GRASP55

50 IB: β-actin

1 2

IgG anti MT1-MMP

B

60 50 40

IB: GRASP55

1

– +

+

2 kDa

GRASP55F MT1/MYC

IP: FLAG IB: MYC

kDa 60

C

IB: MYC

IB: FLAG

Input lysates 60

60

1 2 3 4

Fig 1 MT1-MMP co-immunoprecipitates with GRASP55F (A) Pro-tein extracts prepared from HT1080 cells transiently transfected with pCDNA3.1 Zeo+ (lane 1) or full-length MT1-MMP construct were analyzed by IB with antibodies directed against MT1-MMP, GRASP55 and b-actin (B) Protein extract prepared from HT1080 transiently transfected with MT1-MMP were immunoprecipitated with rabbit control IgGs (lane 1) or with the rabbit polyclonal anti-body directed against MT1-MMP (lane 2) and analyzed by IB using

a monoclonal antibody to GRASP55 The arrow identifies immuno-precipitated MT1-MMP (C) Protein extracts prepared from HT1080 cells transiently transfected with pCDNA3.1 Zeo+ and MT1/MYC (lane 2), pCDNA3.1 Zeo+ and GRASP55F (lane 3) and MT1/MYC and GRASP55F (lane 4) were immunoprecipitated with the FLAG M2 monoclonal antibody and the associated MT1-MMP was detected by IB using the MYC tag monoclonal antibody Expression

of the transfected construct was monitored in the input lysates using specific antibodies The black arrowhead indicates IgG (immu-noglobulin heavy chain).

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A B C

Fig 2 Subcellular localization of GRASP55 and MT1-MMP in bbHT1080 Fixed and permeabilized bbHT1080 cells were incubated with anti-bodies directed against MT1-MMP (A, D, J), GRASP55 (G, K), TGN46 (E) and giantin (B, H) The co-localization can be observed in yellow in the merged panels (C, F, I, L) Arrowheads depict membranous structures where the proteins co-localize Scale bar = 5 lm.

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immunoprecipitated with nonspecific rabbit IgGs or

with the rabbit polyclonal antibody directed against

MT1-MMP As shown in Fig 1B,

immunoprecipita-tion of MT1-MMP led to the co-precipitaimmunoprecipita-tion of a

small amount of endogenous GRASP55, as detected

by immunoblotting (IB) No GRASP55 was detected

when the pre-immune IgGs were used

Co-precipita-tion between MT1-MMP and GRASP55 was also

observed in HT1080 cells expressing exogenous

Myc-tagged MT1-MMP (MT1/MYC) and FLAG-Myc-tagged

GRASP55 (GRASP55F) (Fig 1C, lane 4) or HeLa

cells (Fig S1) No MT1-MMP was detected in control

immunoprecipitations (Fig 1C, lanes 1–3 and Fig S1)

MT1-MMP co-localizes with GRASP55

The co-immunoprecipitation of MT1-MMP and

GRASP55 prompted us to investigate whether these

two proteins co-localized in the same membranous

compartment To investigate this, we used HT1080 cells

stably expressing wild-type MT1-MMP (bbHT1080) In

these cells, MT1-MMP (Fig 2A, 2D) co-localized

extensively with the medial Golgi marker giantin (Fig 2B) and with the trans-Golgi network (TGN) membrane protein marker TGN46 (Fig 2E) Endoge-nous GRASP55 (Fig 2G, 2K) was also found to co-localize with giantin (Fig 2H) [40] and a clear co-localization with MT1-MMP (Fig 2J) could also be observed (Fig 2L) in these cells The co-localization of MT1-MMP and GRASP55 was next assessed using live video microscopy We generated an enhanced yellow fluorescent protein (EYFP)-tagged MT1-MMP con-struct (MT1/EYFP), where the EYFP tag replaced the entire MT1-MMP catalytic domain In HT1080, the intracellular trafficking of MT1/EYFP was indistin-guishable from that of wild-type MT1-MMP and both constructs were found to accumulate in the Golgi appa-ratus and the TGN in these cells (C Roghi, unpublished data) HT1080 cells were then transiently co-transfected with MT1/EYFP and the GRASP55-green fluorescent protein (GFP) fusion protein as previously described [35] and the localization of both proteins was studied in live cells Separation of the GFP and EYFP signals was achieved using a Zeiss META confocal microscope (see

Fig 3 Co-localization of MT1-MMP and GRASP55 in live cells Four consecutive frames (4 s apart) of time lapse sequence collected from HT1080 co-transfected cells with EYFP/MT1 and GRASP55-GFP The arrowheads are examples of dynamic vesicles containing both fluore-scent proteins MT1/EYFP was pseudo-coloured in red during post-acquisition processing The co-localization between GRASP55-GFP and MT1/EYFP can be observed in yellow in the merged panels Scale bar = 16 lm.

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VP16-MT1 VP16

PGGGFFAAAHGTPRRLLYCQRSLLDKV

VP16

VP16-MT1 FRR

A

PGGGFFFRRAAAPRRLLYCQRSLLDKV

VP16

VP16-MT1 HGT

PGGGFFFRRHGTAAALLYCQRSLLDKV

VP16

VP16-MT1 PRR

PGGGFFFRRHGTPRRAAACQRSLLDKV

VP16

VP16-MT1 LLY

PGGGFFFRRHGTPRRLLYAAASLLDKV

VP16

VP16-MT1 CQR

PGGGFFFRRHGTPRRLLYCQRAAADKV

VP16

VP16-MT1 SLL

PGGGFFFRRHGTPRRLLYCQRSLLAAA

VP16

VP16-MT1 DKV

B

KHCEWCRALICRHEKPSALLKGRTACCHSETVV

VP16-TGF- α VP16

PGGGFFFRRHGTPRRLLYCQRSLLAAA

VP16

VP16 MT1 DKV VP16-MT1 Y VP16PGGGFFFRRHGTPRRLLACQRSLLDKV

VP16-MT1 LL VP16 PGGGFFFRRHGTPRRAAYCQRSLLDKV

500

0 100 200 300 400

500

0 100 200 300 400

Luminescence (arbitrary units)

1 2 3 4

GAL4 GRASP55 VP16

MT1

VP16

GAL4 GAL4 GRASP55 VP16 MT1

GAL4 + VP16

+ + +

C

VP16

+

GAL4 GRASP55

+ VP16 TGF- α GAL4

+

GAL4 VP16 1

2 3 Luminescence (arbitrary units)

GAL4 GRASP55 + VP16 TGF- α 4

Fig 4 MT1-MMP interaction with

GRASP55 (A) Schematic representation of

VP16-TGF-a, VP16-MT1 and the VP16-MT1

mutant constructs The mutated amino

acids are shown in bold and the PGGG

linker is shown in italics (B) Interaction

between full-length GRASP55

(GAL4-GRASP55) and MT1-MMP ICD (VP16-MT1)

or (C) TGF-a ICD (VP16-TGF-a) using the

M2H assay.

+ VP16 MT1

GAL4

500

0 100 200 300 400 1

Luminescence (arbitrary units)

A

B

GAL4 GRASP55 + VP16 MT1 FRR

GAL4 GRASP55 + VP16 MT1 HGT

GAL4 GRASP55 + VP16 MT1 PRR

GAL4 GRASP55 + VP16 MT1

GAL4 GRASP55 + VP16 MT1 LLY

2 3 4 5 6

+

GAL4 GRASP55 + VP16 MT1 CQR

GAL4 GRASP55 + VP16 MT1 SLL

+

GAL4 GRASP55 VP16 MT1 DKV

7 8 9

MT1/MYC +

+

+ + + +

MT1 LLY/MYC

IP: FLAG IB: MYC 50

– –

WB: MYC

WB: FLAG

Input lysates

60

60

Fig 5 The LLY motif in the MT1-MMP ICD

is crucial for the interaction with GRASP55.

(A) Interaction between GAL4-GRASP55 and

VP16-MT1 or MT1-MMP ICD triple mutants.

(B) Cell lysates prepared from HT1080 cells

transfected with pCDNA3.1 Zeo+ and MT1/

MYC (lane 1), pCDNA3.1 Zeo+ and

GRASP55F (lane 2), pCDNA3.1 Zeo+

and MT1 LLY/MYC (lane 3), GRASP55F and

MT1 LLY/MYC (lane 4) and GRASP55F

and MT1/MYC (lane 5) were

immunoprecipi-tated with the FLAG M2 antibody.

MT1-MMP present in the

immunoprecipi-tate was detected by IB using the MYC tag

antibody Levels of transfected proteins

were monitored in input lysates using

specific antibodies.

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Materials and methods) As previously described in

fixed bbHT1080 (Fig 2), we clearly observed, in live

HT1080 cells, the presence of both tagged proteins in

the same membrane compartment (Fig 3, merged), thus

confirming the results that were observed previously in

fixed bbHT1080 cells (Fig 2) Interestingly, we also

noted that MT1/EYFP and GRASP55-GFP also

co-localized in very dynamic unidentified cytoplasmic

membranous structures (Fig 3, arrowheads)

MT1-MMP intracellular domain is involved in the

interaction with GRASP55

If the co-immunoprecipitation between MT1-MMP and

GRASP55 is functionally relevant, there should be an

interaction between the peripheral scaffolding protein

and the ICD of MT1-MMP To investigate this, we used

an M2H system MT1-MMP ICD flanked by an

N-ter-minal PGGG linker was fused to the VP16 activation

domain (VP16-MT1; Fig 4A) and full-length

GRASP55 was fused to the GAL4 DNA binding

domain (GAL4-GRASP55) Both constructs were

tran-siently co-transfected in HT1080 cells together with the

reporter plasmid pG5luc, which contains the firefly

lucif-erase gene under the control of five GAL4 binding sites

After 24 h of transfection, the firefly luciferase activity

was measured, as described in the Materials and

meth-ods, and the values obtained were normalized according

to transfection efficiency using the Renilla reniformis

luciferase expressed by the pBIND vector

Co-expres-sion of VP16-MT1 and GAL4-GRASP55 fusion

proteins (Fig 4B, lane 4) in HT1080 resulted in the

production of significantly higher firefly luciferase lumi-nescence compared to the controls (Fig 4B, lanes 1–3), demonstrating an interaction between the MT1-MMP ICD and GRASP55 in the M2H system Using this assay, we also observed an interaction between the VP16-TGF-a ICD (Fig 4A) and GAL4-GRASP55 (Fig 4C, lane 4), therefore confirming the interaction of these two proteins previously observed biochemically [37] or using a yeast two-hybrid assay [39] Interestingly,

in the M2H system, the interaction between GRASP55 and TGF-a ICD did not require the oligomerization of the TGF-a ICD as previously observed using a yeast two-hybrid assay [39]

The MT1-MMP LLY motif is important for the interaction with GRASP55

We next sought to define the nature of the GRASP55 binding site in the MT1-MMP ICD pACT plasmids driving the expression of MT1-MMP ICDs containing single-, double- and triple-point mutations were gener-ated (Fig 4A) and used in the M2H system System-atic analysis of the interaction between the triple MT1-MMP ICD mutants and GAL4-GRASP55 revealed that, apart from the VP16-MT1 FFR (Fig 5A, lane 3) and VP16-MT1 DKV mutants (Fig 5A, lane 9), all the other triple mutants (Fig 5A, lanes 4–8) displayed a marked and significant reduc-tion of luciferase activity compared to the wild-type VP16-MT1 construct (Fig 5A, lane 2) In particular, the mutation of the LLY573 motif (LLY571-573AAA) (Fig 5A, lane 6) resulted in a complete inhibition of

MT3 MT3 ILY MT5

VP16-MT1

VP16-MT2

PGGGFFFRRHGTPRRLLYCQRSLLDKV

VP16

PGGGVQMQRKGAPRVLLYCKRSLQEWV

VP16

% homology with MT1-MMP ICD -57.1%

VP16-MT3

VP16-MT5

PGGGFQFKRKGTPRHILYCKRSMQEWV

VP16

PGGGFQFKNKTGPQPVTYYKRPVQEWV

VP16

57.1%

23.8%

500

A

B Luminescence (arbitrary units)

0 100 200 300 400

+

GAL4 VP16

+

GAL4 GRASP55 VP16

+

GAL4 GRASP55 VP16

4 5 6

+

GAL4 VP16

GAL4 GRASP55 + VP16

+

GAL4 GRASP55 VP16

1 2 3

GAL4 GRASP55 VP16

+

GAL4 VP16

+

GAL4 GRASP55 MT5 VP16

+

GAL4 GRASP55 VP16 MT5 VTY

7 8 9

MT2

MT3

MT2 MT2 LLY

Fig 6 The MT2-MMP LLY motif is involved

in the interaction with GRASP55 (A) Schematic representation of the VP16-MT1, VP16-MT2, VP16-MT3 and VP16-MT5 constructs Amino acids conserved between MT1-MMP ICD and either MT2-, MT3- or MT5-MMP are shown in bold (B) Interactions between GAL4-GRASP55 and VP16-MT2, VP16-MT2 LLY, VP16-MT3, VP16-MT3 ILY, VP16-MT5 and VP16-MT5 VTY were tested using the M2H system.

**P < 0.001.

Trang 8

the interaction between MT1-MMP ICD and

GAL4-GRASP55 IB analysis revealed that all triple

mutants were expressed to a similar level (data not

shown), indicating that the differences in interaction

observed were not a result of impaired protein

produc-tion or stability Our data therefore suggest that most

of the MT1-MMP ICD is implicated in the interaction

with GRASP55, with the LLY573motif playing a

criti-cal role in the interaction between the two proteins

A reduction of luciferase activity was also observed

using the VP16-MT1 Y (MT1Y573A) (Fig S2, lane 5)

and VP16-MT1 LL (LL570-572AA) mutants (Fig S2,

lane 4), although not to the level observed with the

LLY570-573AAA triple mutant (Fig S2, lane 3),

dem-onstrating that the mutation of the whole LLY573

motif is needed to abolish the interaction of

MT1-MMP ICD with GRASP55

The importance of the LLY573 motif in the

MT1-MMP ICD observed in the M2H assay was next

con-firmed by co-immunoprecipitation HT1080 cells were

transiently co-transfected with GRASP55F together

with MT1/MYC or MT1 LLY/MYC (LLY570-573

AAA) triple mutant and total cell lysates were

subjected to immunoprecipitation using the FLAG tag

monoclonal antibody As previously observed, we

detected a clear interaction between GRASP55F and

the wild-type MYC-tagged MT1-MMP (Fig 5B, lane

5) when both proteins were expressed in HT1080 cells

Mutation of the LLY573 motif to AAA573 in

MT1-MMP ICD led to a marked reduction in the amount

of MT1-MMP present in the immunoprecipitated

material (Fig 5B, lane 4), thus confirming the

impor-tant role of the LLY573 motif in the interaction

between the protease and GRASP55 Interestingly,

mutation of the LLY573 motif led to the detection

of pro-MT1-MMP in the immunoprecipitate,

sugges-ting that the disruption of the interaction between MT1-MMP and GRASP55 could affect the activation

of the protease

Taken together, and having been obtained using dif-ferent experimental approaches, our data demonstrate that the LLY573 motif in MT1-MMP ICD plays an important role in the interaction between MT1-MMP with GRASP55 Interestingly, we were unable to co-immunoprecipitate MT1-MMP and the soluble G2A GRASP55F mutant (Fig S3) [35,37,41], suggest-ing that the Golgi localization of GRASP55 is crucial for its interaction with MT1-MMP

GRASP55 interacts with MT2-, MT3- and MT5-MMP

The sequences of cytoplasmic domains of the four MT-MMPs are conserved (Fig 6A) Interestingly, the LLY573 motif in MT1-MMP ICD was completely conserved in MT2-MMP (LLY660), whereas ILY598 and VTY636 sequences were found in MT3-MMP and MT5-MMP ICDs, respectively (Fig 6A) To test whether MT2-, MT3- and MT5-MMP ICDs could also interact with GRASP55, we generated VP16-MT2, -MT3 and -MT5 chimeras (Fig 6A) As shown in Fig 6B, all three ICDs (Fig 6B, lanes 2, 5 and 8) showed a clear interaction with GRASP55 We also tested whether the LLY660 motif in MT2-MMP, the ILY598 motif in MT3-MMP or the VTY636 motif in MT5-MMP could also be involved in the interaction with GRASP55 Accordingly, MT2 LLY, VP16-MT3 ILY and VP16-MT5 VTI triple mutants were generated and used in the M2H assay As previously observed for MT1-MMP, mutation of the MT2-MMP LLY660 motif to AAA660 significantly decreased the interaction with GRASP55 (Fig 6B, lane 3) By

Luminescence (arbitrary units)

500

0 100 200 300 400

+ VP16 MT1 GAL4

VP16

+

GAL4 GRASP55 GAL4 GRASP55 + VP16 MT1 P1

GAL4 + VP16 MT1

+ VP16 MT1 GAL4 P2

+ VP16 MT1 GAL4

1 2 3 4 5 6

+ VP16 MT1

+ VP16 TGF-α GAL4

+

GAL4 GRASP55 VP16

Luminescence (arbitrary units)

500

0 100 200 300 400 1

2

+

GAL4 GRASP55 VP16

+

P1 GAL4 VP16 TGF-α

2 3 TGF-α

A

B

R3

Fig 7 GRASP55 PDZ2 and region 3 are

important for the interaction with the

MT1-MMP ICD (A) Interactions between

VP16-MT1 and GAL4-GRASP55, GRASP55

PDZ1 (GAL4-P1), GRASP55 PDZ2 (GAL4-P2)

or GRASP55 region 3 (GAL4-R3) and

(B) between VP16-TFG a and

GAL4-GRASP55 or GAL4-P1 were tested using

the M2H system.

Trang 9

contrast, mutation of MT3-MMP ILY598 (Fig 6B,

lane 6) and MT5-MMP VTY636to AAA (Fig 6B, lane

9) had no effect on GRASP55 binding

MT1-MMP ICD binds to PDZ2 domain and

region 3 of GRASP55

GRASP55 contains two non-overlapping and

structur-ally independent PSD-95/SAP90 Drosophila septate

junction protein discs-large and epithelial tight junction

ZO-1 (PDZ) domains in its N-terminal half, followed

by a third region of approximately 250 amino acids

without known structural motif (region 3) We next

aimed to identify the region(s) of GRASP55 that

inter-acts with MT1-MMP ICD GRASP55 PDZ1 (amino

acids 1–107), GRASP55 PDZ2 (amino acids 84–172)

and GRASP55 region 3 (amino acids 173–454) were

each fused to the GAL4 DNA binding domain and

used together with VP16-MT1 in the M2H system

MT1-MMP ICD was found to interact with full-length

GRASP55 (Fig 7A, lane 3), as well as with GRASP55

PDZ2 (P2; Fig 7A, lane 5) and GRASP55 region 3

(R3; Fig 7A, lane 6) However, no interaction was

found between VP16-MT1 and GAL4-GRASP55 PDZ1 (P1; Fig 7A, lane 4), despite the expression of the GAL4-GRASP55 PDZ1 chimera in HT1080 (data not shown) TGF-a was previously reported to co-immunoprecipitate with a very small amount of flagged tagged GRASP55 PDZ1 domain [37] In our hands, no interaction between TGF-a ICD and GRASP55 PDZ1 could be observed in the M2H assay (Fig 7B, lane 3) The lack of interaction could result from a mis-folding

of GRASP55 PDZ1 subsequent to its fusion to the GAL4 DNA binding domain We therefore cannot rule out an interaction between MT1-MMP ICD and the GRASP55 PDZ1 domain

GRASP55 binds to furin, PC5/6B and PC7 intracellular domains

The pro-convertase furin has previously been impli-cated in the activation of pro-MT1-MMP [42] Because MT1-MMP activation occurs during the intracellular traffic of the protease, we tested whether furin could interact, via its ICD, with GRASP55 Accordingly, we generated a VP16-furin construct

500

0 100 200 300 400

+ VP16 Furin

GAL4

Luminescence (arbitrary units)

2 3 4 5 6 GAL4 + VP16 PC7

+

GAL4 VP16 PC5/6B

GAL4 GRASP55 + VP16 Furin

GAL4 GRASP55 + VP16 PC5/6B

PC7

VP16

GAL4 GRASP55 +

Luminescence (arbitrary units)

+

GAL4 VP16 Furin

+

GAL4 GRASP55 VP16

GAL4 GRASP55 + VP16 Furin

P1

GAL4 + VP16 Furin

500

0 100 200 300 400 1

2 3 4

+

GAL4 P2 VP16 Furin

+

R3

GAL4 VP16 Furin

5 6

A

B

C

Furin GRASP55

Fig 8 GRASP55 interacts with furin, PC5/ 6B and PC7 (A) Interactions between GAL4-GRASP55 and furin, PC5/6B or PC7 ICDs were tested using the M2H system (B) Interaction between VP16-furin and GAL4-GRASP55, GRASP55 PDZ1 (GAL4-P1), GRASP55 PDZ2 (GAL4-P2) or GRASP55 Region 3 (GAL4-R3) (C) Furin co-localized with GRASP55 bbHT1080 cells, transfected with a full-length furin cDNA, were permeabilized and stained with polyclonal antibodies against furin and GRASP55 Arrows show examples of membrane compartment containing GRASP55 and furin Scale bar = 10 lm.

Trang 10

where the furin ICD was fused to VP16 We also

generated the VP16-PC5/6B and VP16-PC7 chimeras

where the ICDs of PC5/6B and PC7 type I

trans-membrane pro-convertases were also fused to VP16

Comparable to furin, PC5/6B and PC7 have

previ-ously been reported to process tetrabasic cleavage

sites [43] and their roles in pro-MT1-MMP activation

have been suggested both in vitro [44] and in vivo [42]

As shown in Fig 8A, a clear interaction between

furin ICD and GRASP55 could be observed (Fig 8A,

lane 2) compared to the control (Fig 8A, lane 1) We also observed a significant interaction between GRASP55 and PC5/6B (Fig 8A, lane 4) or PC7 (Fig 8A, lane 6) ICDs We next tested the interaction between furin ICD and the GRASP55 domain con-structs described previously As shown in Fig 8B, we detected an interaction between furin ICD and PDZ2 (Fig 8B, lane 5) and region 3 (Fig 8B, lane 6) of GRASP55 No interaction was detected between GRASP55 PDZ1 (Fig 8B, lane 4) and furin ICD,

A

GRASP55F Furin

IP: MT1-MMP IB: Furin

kDa 98 64

*

C

IB: MT1-MMP

EGFP-furin ICD 64

50

kDa

pro-MT1-MMP active-MT1-MMP

IB: FLAG IB: Furin

Input lysate

IB: MT1-MMP 50

64

64

98

50

36

GRASP55F MT1/MYC

EGFP-furin ICD (μg)

B

50

D

IP: FLAG IB: MYC EGFP furin ICD (μg)

60

60 50

kDa

5 10 15 20

n.s

***

IB: FLAG IB: GFP

Input lysate

60 50

60

60

0

5 )

IB: MYC

50

– –

Fig 9 GRASP55 is important for MT1-MMP–furin complex formation and activation of pro-MT1-MMP (A) Lysates of bbHT1080 cells trans-fected with pCDNA3.1 Zeo+ vector control (lane 1), pCDNA3.1 Zeo+ and furin (lane 2), pCDNA3.1 Zeo+ and GRASP55 (lane 3) or with furin and GRASP55F (lane 4) were immunoprecipitated using the affinity-purified anti-MT1-MMP IgGs and the associated furin was detected by

IB Levels of transfected proteins were monitored in input lysates using specific antibodies Asterisks marks endogenous furin immunopre-cipitated by MT1-MMP in bbHT1080 (B) Expression of EGFP-furin ICD disrupted the formation of the complex between MT1-MMP and GRASP55 Lysates of HT1080 cells transfected with pCDNA3.1 Zeo+ vector control (lane 1), MT1/MYC and GRASP55F (lane 2), MT1/MYC and GRASP55F and 0.5 lg EGFP-furin ICD (lane 3) or MT1/MYC and GRASP55F and 1.0 lg of EGFP-furin ICD (lane 4) were immunoprecipi-tated with the FLAG antibody and the associated MT1-MMP was detected by IB using the MYC tag antibody Top black arrowheads indicate IgGs The bottom black arrowhead indicates a crossreaction (C) IB analysis of protein extracts prepared from the EGFP-negative (lane 1) and -positive (lane 2) cell population sorted in Fig S4 Equal amounts of total protein (6 lg) were loaded and the expression of MT1-MMP (pro and active) was analyzed by IB Protein loading was controlled using the b-actin polyclonal antibody (D) Expression of furin decrease MT1-MMP cell surface activity HT1080 cells were transiently transfected with empty vector pCDNA3.1 Zeo+, furin, GRASP55, fu-rin + GRASP55, MT1-MMP, MT1-MMP + fufu-rin, MT1-MMP + GRASP55 and MT1-MMP + GRASP55 + fufu-rin 4b-Phorbol 12-myristate 13-ace-tate was used at 50 ngÆlL)1 After 24 h, supernatants were collected and analyzed by zymography Data represent the mean ± SEM of two independent experiments.

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