CN104120108A - Application of Beclin1 protein acetylation and mutation - Google Patents
Application of Beclin1 protein acetylation and mutation Download PDFInfo
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Abstract
The invention relates to the field of physiology and molecular biology and discloses an acetylation application of Beclin 1. The deacetylase inhibitor can acetylate Beclin1, so that the expression level of Beclin1 is increased, and the autophagy level is improved. And (3) carrying out negative sense mutation on the Beclin1K416 site by adopting a point mutation technology to construct a K416R mutant plasmid. After 293T cells are transfected by the mutant plasmid, the acetylation level is partially reduced, but a more obvious acetylation band still exists. Even so, Beclin1 expression and LC3 expression were significantly reduced, thereby inhibiting the occurrence of autophagy.
Description
Technical field
The present invention relates to physiology and biology field, be specially the acetylizad application of Beclin1.
Background technology
Protein post-translational modification is very important, changes the space structure of protein, thereby affect its function and interaction by the plus-minus of subunit, even affects the stability of protein itself.Common protein post-translational modification comprises phosphorylation, ubiquitination, acetylize, glycosylation etc., and these modifications are determining the activity of some important albumen, in most physiological metabolism paths, plays a part molecular switch.Acetylize refers to after protein translation completes, and increases the modification of ethanoyl by acetyltransferase on protein N terminal residue.Acetylize plays an important role in the stability of protein function and structure.All there is acetylize state in the albumen such as histone, p53, tubulin, at its acetylize state, and Chromatin Protein and metabolizing enzyme high concentration, prompting acetylation modification has sizable effect to genetic expression and metabolism.In bacterium, the protein relevant with center metabolism more than 90% is acetylation, and the scope of prompting acetylation modification is very extensive.Acetylation modification generally occurs in Methionin (K), and in view of state of charge, the amino acid similarity of arginine (R) and deacetylation, therefore, deacetylation state is simulated in conventional Methionin → arginine sudden change (KR sudden change).Generally; acetylization reaction and deacetylation are by histone acetyltransferase (HAT) and deacetylase (HDAC) catalysis; although HAT and HDAC are called as histone acetyltransferase and histon deacetylase (HDAC), in fact they also can be to the nonhistones modification of carrying out acetylize and deacetylation.
Autophagy (Autophagy) is the general biological phenomena being present in eukaryote, is the important channel that organism adaptation external environment changes, safeguards homeostasis.Fundamental research shows, autophagy likely and between the incretion metabolism disease such as diabetes, obesity exists contact.As one of autophagy related gene, Beclin1 is playing the part of important role in the generation of autophagy, the histiocytic physiological metabolism process of wide participation.
Although the effect of Beclin1 in autophagy is most important, its posttranslational modification is also receiving much concern in recent years, so far, also few about the research of Beclin1 posttranslational modification.Most study is the phosphorylation modification of Beclin1 comparatively speaking, have and report the Thr119 site of dead associated protein death-associatedproteinkinase (DAPK) in can phosphorylation Beclin1 protein B H3 territory, impel Beclin1 and BCL2/BCL-XL to dissociate, the Beclin1 of unbound state increases, and autophagy process activates.
Except phosphorylation, the ubiquitination of Beclin1 is also determined and was reported.The ubiquitination of Beclin1 is by ubiquitin K63 mark, TRAF6 is the ubiquitination enzyme of Beclin1 the TRAF binding domains that identifies 2 Beclin1, the K117 site that is arranged in Beclin1 protein B H3 structural domain is the main ubiquitination binding site of K63, is the topmost ubiquitination of Beclin1 site.At scavenger cell, give that inflammatory factor stimulates or amino acid is deprived, can mediate and impel Beclin1 ubiquitination by TRAF6, then dissociate with Bcl-2, activation autophagy approach, and go the effectively autophagy activation of antagonism TRAF6 of ubiquitination enzyme A20.Suppress ubiquitin-specific peptase USP10 and USP13 to Beclin1 go ubiquitination effect, can impel Beclin1 and the degraded of Vps34 mixture, thereby suppress autophagy, occur.
From existing report, there is phosphorylation and ubiquitination in Beclin1, and these two kinds of modifications have all directly affected the autophagy process of Beclin1 mediation.Yet whether Beclin1 can be acetylation it be unclear that.
Summary of the invention
The present invention is intended to the expression with acetylize regulation and control Beclin1 albumen, and regulates and controls the autophagy that Beclin1 albumen mediates.
With deacetylase inhibitor, can make Beclin1 that acetylize occurs, thereby increase the expression amount of Beclin1, improve autophagy level.
The probability that Beclin1K416 site can be acetylation is very high, adopts point mutation technology to carry out negative justice sudden change to Beclin1K416 site, by lysine mutation, is arginine (KR sudden change), thereby has built K416R saltant type plasmid.By after this saltant type plasmid transfection 293T cell, its Acetylation Level has part to reduce, but still has obvious acetylize band.Even so, the expression of Beclin1 and the expression of LC3 significantly reduce, thereby have suppressed the generation of autophagy.
The present invention has determined that Beclin1 can be acetylation.Result demonstration, ACE-Beclin1 place band obviously exists, and along with extend constantly intensification the action time of deacetylase inhibitor NAM+TSA (NT), locates band the most obvious about 6 hours.Thus, there is acetylize state in Beclin1, can be acetylation.
Beclin1 mainly comprises BH3, CC, these 3 structural domains of ECD.BH3 structural domain comprises 105-125 amino acid sites, is the main position of Beclin1 and the combination of BCL2/BCL-XL family, regulates the generation of autophagy and apoptotic process by the combination with the anti-autophagy albumen of these anti-apoptosis.CC structural domain has participated in Beclin1 and UVRAG, ATG14/Barkor etc. and has formed dimer, and these mixtures play an important role in the generation of autophagy.ECD has occupied the approximately amino acid of half of Beclin1C end, the structural domain of this structural domain and current known every other protein does not all have homology, but almost participated in all functions of Beclin1, so ECD mechanism may be a breach of decoding the new function of Beclin1.The ECD structural domain of narrow sense comprises 244-337 amino acid sites, and the ECD structural domain of broad sense comprises whole 1/2 Beclin1C terminal amino acid.According to the latter's definition, the K416 site the present invention relates to is positioned at the ECD structural domain of Beclin1, is likely bearing new function.Although the acetylize of Beclin1 is not blocked in K416R sudden change completely, on producing of the protein content of Beclin1 and autophagy larger impact.Compare with the Beclin1 of wild-type (WT), the Beclin1 protein expression of K416R sudden change significantly declines.
Accompanying drawing explanation
Fig. 1 is the acetylize timeliness of Beclin1 under deacetylase inhibitor NT effect
Fig. 2 is that K416R sudden change is on the acetylizad impact of Beclin1
Fig. 3 is the protein expression situation of Beclin1 after 293T cell untransfected (CON), transfection wild-type (WT) and saltant type (K416R) Beclin1 plasmid
Fig. 4 is the proteolytic degradation of the Beclin1 with observing after defence line bacterium ketone (CHX) effect
Fig. 5 is that the expression of the cell LC3 of transfection K416RBeclin1 plasmid changes
Fig. 6 is the impact of P300/PCAF/SIRT1-7 on Beclin1 protein content
Embodiment
Embodiment 1
Because the acetylize of Beclin1 not yet has clearly report, so Beclin1 does not exist business-like acetylize antibody yet.We adopt the method for IP to detect the acetylize of Beclin1.With deacetylase inhibitor NT (NAM+TSA) effect 293T cell, we have observed the acetylize of Beclin1, and along with action time of NT extending to 6 hours, the Acetylation Level of Beclin1 is also in continuous increase.The acetylize timeliness of the lower Beclin1 of NT effect is as Fig. 1.
The expression amount of Beclin1 obviously raises, and prompting may be the stability that the acetylize of Beclin1 has affected its albumen itself.
Embodiment 2
After adopting deacetylase inhibitor NAM niacinamide and TSA Trichostatin A (NT) effect 293T cell, the expression amount of Beclin1 obviously raises, and prompting may be the stability that the acetylize of Beclin1 has affected its albumen itself.Method by immunoprecipitation (IP) is further determined the acetylize state of Beclin1, and studies its acetylize site by the method for KR point mutation.
Predict the acetylize site of Beclin1 the ASEB acetylize site estimation website that employing is established by Peking University, the demonstration that predicts the outcome, and the probability that Beclin1K416 site can be acetylation is very high.Therefore, we adopt point mutation technology to carry out negative justice sudden change to Beclin1K416 site, by lysine mutation, are arginine (KR sudden change), thereby have built K416R saltant type plasmid.To after this saltant type plasmid transfection 293T cell, use its Acetylation Level of IP technology for detection; find to compare with wild-type (WT) plasmid; the Acetylation Level of K416R saltant type plasmid has part to reduce; but still there is obvious acetylize band; this explanation K416R may be one of acetylize site of Beclin1, but its topmost acetylize site not necessarily.
Although K416 does not block the acetylize of Belicn1 completely; but; produce very interesting phenomenon; K416R saltant type plasmid proceeds to after 293T cell; the expression of the Beclin1 that can detect and the expression of LC3 significantly reduce; as Fig. 2, i.e. the sudden change in this site may affect the stability of Beclin1, thereby has further had influence on the generation of autophagy.Figure 3 shows that the protein expression situation of Beclin1 after 293T cell untransfected (CON), transfection wild-type (WT) and saltant type (K416R) Beclin1 plasmid, the expression of visible 6 hours K416RBeclin1 is starkly lower than WTBeclin1, and more obviously low at 8 hours.
Fig. 4 is the proteolytic degradation of the Beclin1 with observing after defence line bacterium ketone (CHX) effect, and the transformation period of visible K416RBeclin1 is starkly lower than WTBeclin1.Fig. 5 in the cell of transfection K416RBeclin1 plasmid, compares with wild-type (WT) as seen, and the expression of LC3 obviously reduces, and autophagy process is suppressed.
Embodiment 3
SIRTUIN family is a class deacetylase, and that finds at present mainly comprises SIRT1-7.P300 and PCAF are common acetylases.Whether we detect the protein content of Beclin1 after 293T cell transfecting SIRT1-7, P300, PCAF by WesternBlot, to observe it, the expression amount of Beclin1 is exerted an influence.Preliminary result shows, after P300 and PCAF transfection, do not observe the considerable change of Beclin1, and after SIRT6 transfection, the expression amount of Beclin1 obviously reduces, and other SIRTUIN family members are on the not impact of the expression amount of Beclin1.
Fig. 6 shows, repeatedly after transfection, finds the expression amount of corresponding protein after each plasmid transfection inconsistent, and this may, with the purity of different plasmids, the size of object fragment etc. are relevant, likely can produce certain impact to result.Visible deacetylase, especially SIRT6, can affect the acetylize of Beclin1, thereby suppress autophagy.
The present invention first adopts the method for IP to determine whether Beclin1 can be acetylation.Result demonstration, ACE-Beclin1 place band obviously exists, and along with extend constantly intensification the action time of deacetylase inhibitor NAM+TSA (NT), locates band the most obvious about 6 hours.Thus, there is acetylize state in Beclin1, can be acetylation.After determining that Beclin1 can be acetylation, we find the acetylize site of Beclin1 then.The prediction in acetylize site has several different methods, and LC/LC-MS/MS mass spectroscopy is the method for relatively commonly using, but cost is higher, and actually operating has certain difficulty.Use software or website prediction relatively simple, but false positive rate is higher.After site mutation, further carry out IP experimental analysis, could determine whether this site is acetylize site.When the acetylize site of prediction Beclin1; the ASEB website that has adopted team of Peking University to create; predict the probability that Beclin1K416 site is acetylation higher; so adopt the method for fixed point point mutation to carry out the negative justice sudden change of KR to this site, attempt to simulate the deacetylation state of Beclin1.Result demonstration, after this site mutation, the acetylize state of Beclin1 slightly reduces, but not fairly obvious, illustrates that this site may participate in the acetylation modification of Beclin1, but is not main site.However, this site mutation can make Beclin1 protein expression significantly decline.
Claims (3)
- The acetylize of 1.Beclin1 albumen is used for suppressing autophagy.
- 2.Beclin1 the K416R site mutation of albumen is used for suppressing autophagy.
- 3.SIRT6 acetylase is for suppressing the protein mediated autophagy of Beclin1.
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Cited By (3)
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| CN107540737A (en) * | 2016-06-29 | 2018-01-05 | 香港理工大学 | For promoting the biodegradable hydrocarbon stapler peptide of interior body and lysosome |
| CN109738506A (en) * | 2019-01-10 | 2019-05-10 | 青岛大学附属医院 | Autophagy GAP-associated protein GAP acetylation sites research method in a kind of mature fat cell |
| CN112029738A (en) * | 2020-08-18 | 2020-12-04 | 浙江省人民医院 | Human parkin protein acetylation and application thereof in medicine preparation |
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Cited By (4)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN107540737A (en) * | 2016-06-29 | 2018-01-05 | 香港理工大学 | For promoting the biodegradable hydrocarbon stapler peptide of interior body and lysosome |
| CN109738506A (en) * | 2019-01-10 | 2019-05-10 | 青岛大学附属医院 | Autophagy GAP-associated protein GAP acetylation sites research method in a kind of mature fat cell |
| CN112029738A (en) * | 2020-08-18 | 2020-12-04 | 浙江省人民医院 | Human parkin protein acetylation and application thereof in medicine preparation |
| CN112029738B (en) * | 2020-08-18 | 2022-04-29 | 浙江省人民医院 | Human parkin protein acetylation and application thereof in medicine preparation |
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