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| 1 | LRIF1 interacts with HPla to coordinate accurate chromosome segregation during mitosis显示文摘Heterochromatin protein 1α (HP1α)regulates chromatin specification and plasticity during cell fate decision.Different structural determinants account for HP1α Localization and function during cell division cycle.Our earlier study showed that centromeric Localization of HP1α depends on the epigenetic mark H3K9me3 in interphase,while its centromeric location in mitosis relies on uncharacterized PXVXL-containing factors.Here,we identified a PXVXL-containing protein,Ligand-dependent nuclear receptorinteracting factor 1 (LRIF1),which recruits HPla to the centromere of mitotic chromosomes and its interaction with HP1α is essential for accurate chromosome segregation during mitosis.LRIF1 interacts directly with HPla chromoshadow domain via an evolutionariLy conserved PXVXL motif within its C-terminus.Importantly,the LRIF1-HPla interaction is critical for Aurora B activity in the inner centromere.Mutation of PXVXL motif of LRIF1 Leads to defects in HPla centromere targeting and aberrant chromosome segregation.These findings reveal a previously unrecognized direct Link between LRIF1 and HP1α in centromere plasticity control and illustrate the critical role of LRIF1-HP1α interaction in orchestrating accurate cell division. | Saima Akram Fengrui Yang Junying Li Gregory Adams Yingying Liu Xiaoxuan Zhuang Lingluo Chu Xu Liu Nerimah Emmett Winston Thompson McKay Mullen Saravana Muthusamy Wenwen Wang Fei Mo Xing Liu | 2018 | Journal of Molecular Cell Biology2018，10，6： | 5 |
| 2 | Acetytation of ACAP4 regutates CCL18-elicited breast cancer cell migration and invasion显示文摘Tumor metastasis represents the main causes of cancer-related death.Our recent study showed that chemokine CCL18 secreted from tumor-associated macrophages regulates breast tumor metastasis,but the underlying mechanisms remain less clear.Here, we show that ARF6 GTPase-activating protein ACAP4 regulates CCL18-elicited breast cancer cell migration via the acetyltransferase PCAF-mediated acetylation.CCL18 stimulation elicited breast cancer cell migration and invasion via PCAF-dependent acetylation.ACAP4 physically interacts with PCAF and is a cognate substrate of PCAF during CCL18 stimulation.The acetylation site of ACAP4 by PCAF was mapped to Lys311 by mass spectrometric analyses.Importantly,dynamic acetylation of ACAP4 is essential for CCL18-induced breast cancer cell migration and invasion,as overexpression of the persistent acetylation-mimicking or nonacetylatable ACAP4 mutant blocked CCL18-elicited cell migration and invasion.Mechanistically,the acetylation of ACAP4 at Lys311 reduced the lipid-binding activity of ACAP4 to ensure a robust and dynamic cycling of ARF6-ACAP4 complex with plasma membrane in response to CCL18 stimulation.Thus,these results present a previously undefined mechanism by which CCL18-elicited acetylation of the PH domain controls dynamic interaction between ACAP4 and plasma membrane during breast cancer cell migration and invasion. | Xiaoyu Song Wei Liu Xiao Yuan Jiying Jiang Wanjuan Wang McKay Mullen Xuannv Zhao Yin Zhang Fusheng Liu Shihao Du Adeel Rehman Ruijun Tian Jian Li Andra Frost Zhenwei Song Hadiyah-Nicole Green Calmour Henry Xing Liu Xia Ding Dongmei Wang Xuebiao Yao | 2018 | Journal of Molecular Cell Biology2018，10，6： | 3 |
| 3 | Modeling of COVID-19 disease disparity in gastric organoids reveals the spatiotemporal dynamics of SARS-CoV-2 infectivity显示文摘Dear Editor,The promptness and continuous expansion of the coronavirus disease 2019(COVID-19)pandemic,elicited by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)and its variants,has presented an unprecedented impact on human health(WHO Coronavirus(COVID-19)Dashboard,2021).Although vaccination has attenuated the severe symptoms,there is no specific antiviral medication available for preventing the viral spread(Drayman et al.,2021). | Wenwen Wang Fengrui Yang Jie Lin Saravanakumar Muthusamy Shihao Du McKay Mullen Fatima Garba Wanjuan Wang Xu Liu Tao Li Zhihong Yang Xia Ding Felix Aikhionbare Xinjiao Gao Zhikai Wang Xing Liu Xuebiao Yao | 2022 | Journal of Molecular Cell Biology2022，14，2： | 1 |
| 4 | Acetylation of ezrin regulates membrane–cytoskeleton interaction underlying CCL18-elicited cell migration显示文摘Ezrin,a membrane–cytoskeleton linker protein,plays an essential role in cell polarity establishment,cell migration,and division.Recent studies show that ezrin phosphorylation regulates breast cancer metastasis by promoting cancer cell survivor and promotes intrahepatic metastasis via cell migration.However,it was less characterized whether there are additional post-translational modifications and/or post-translational crosstalks on ezrin underlying context-dependent breast cancer cell migration and invasion.Here we show that ezrin is acetylated by p300/CBP-associated factor(PCAF)in breast cancer cells in response to CCL18 stimulation.Ezrin physically interacts with PCAF and is a cognate substrate of PCAF.The acetylation site of ezrin was mapped by mass spectrometric analyses,and dynamic acetylation of ezrin is essential for CCL18-induced breast cancer cell migration and invasion.Mechanistically,the acetylation reduced the lipid-binding activity of ezrin to ensure a robust and dynamic cycling between the plasma membrane and cytosol in response to CCL18 stimulation.Biochemical analyses show that ezrin acetylation prevents the phosphorylation of Thr567.Using atomic force microscopic measurements,our study revealed that acetylation of ezrin induced its unfolding into a dominant structure,which prevents ezrin phosphorylation at Thr567.Thus,these results present a previously undefined mechanism by which CCL18-elicited crosstalks between the acetylation and phosphorylation on ezrin control breast cancer cell migration and invasion.This suggests that targeting PCAF signaling could be a potential therapeutic strategy for combating hyperactive ezrin-driven cancer progression. | Xiaoyu Song Wanjuan Wang Haowei Wang Xiao Yuan Fengrui Yang Lingli Zhao McKay Mullen Shihao Du Najdat Zohbi Saravanakumar Muthusamy Yalei Cao Jiying Jiang Peng Xia Ping He Mingrui Ding Nerimah Emmett Mingming Ma Quan Wu Hadiyah-Nicole Green Xia Ding Dongmei Wang Fengsong Wang Xing Liu | 2020 | Journal of Molecular Cell Biology2020，12，6： | 1 |
| 5 | Dynamic phosphorylation of CENP-N by CDK1 guides accurate chromosome segregation in mitosis显示文摘In mitosis,accurate chromosome segregation depends on the kinetochore,a supermolecular machinery that couples dynamic spin-dle microtubules to centromeric chromatin.However,the structure–activity relationship of the constitutive centromere-associated network(CCAN)during mitosis remains uncharacterized.Building on our recent cryo-electron microscopic analyses of human CCAN structure,we investigated how dynamic phosphorylation of human CENP-N regulates accurate chromosome segregation.Our mass spectrometric analyses revealed mitotic phosphorylation of CENP-N by CDK1,which modulates the CENP-L–CENP-N interaction for accurate chromosome segregation and CCAN organization.Perturbation of CENP-N phosphorylation is shown to prevent proper chromosome alignment and activate the spindle assembly checkpoint.These analyses provide mechanistic insight into a previously undefined link between the centromere–kinetochore network and accurate chromosome segregation. | Ran Liu Zhen Dou Tian Tian Xinjiao Gao Lili Chen Xiao Yuan Chunyue Wang Jiahe Hao Ping Gui McKay Mullen Felix Aikhionbare Liwen Niu Guoqiang Bi Peng Zou Xuan Zhang Chuanhai Fu Xuebiao Yao Jianye Zang Xing Liu | 2023 | Journal of Molecular Cell Biology2023，15，6： | 0 |
| 6 | Phosphorylation of CENP-R by Aurora B regulates kinetochore-microtubule attachment for accurate chromosome segregation显示文摘Error-free mitosis depends on accurate chromosome attachment to spindle microtubules via a fine structure called the centromere that is epigenetically specified by the enrichment of CENP-A nucleosomes.Centromere maintenance during mitosis requires CENP-A-mediated deposition of constitutive centromere-associated network that establishes the inner kinetochore and connects centromeric chromatin to spindle microtubules during mitosis.Although previously proposed to be an adaptor of retinoic acid receptor,here,we show that CENP-R synergizes with CENP-OPQU to regulate kinetochore-microtubule attachment stability and ensure accurate chromosome segregation in mitosis.We found that a phospho-mimicking mutation of CENP-R weakened its localization to the kinetochore,suggesting that phosphorylation may regulate its localization.Perturbation of CENP-R phosphorylation is shown to prevent proper kinetochore-microtubule attachment at metaphase.Mechanistically,CENP-R phosphorylation disrupts its binding with CENP-U.Thus,we speculate that Aurora B-mediated CENP-R phosphorylation promotes the correction of improper kinetochore-microtubule attachment in mitosis.As CENP-R is absent from yeast,we reasoned that metazoan evolved an elaborate chromosome stability control machinery to ensure faithful chromosome segregation in mitosis. | Divine Mensah Sedzro Xiao Yuan McKay Mullen Umer Ejaz Tongtong Yang Xu Liu Xiaoyu Song Yun-Chi Tang Weijun Pan Peng Zou Xinjiao Gao Dongmei Wang Zhikai Wang Zhen Dou Xing Liu Xuebiao Yao | 2022 | Journal of Molecular Cell Biology2022，14，7： | 0 |
| 7 | Article Navigation Syntelin inhibits triple-negative breast cancer cell proliferation and metastasis显示文摘Dear Editor,The hallmarks of cancer comprise several distinct biological characteristics acquired during the multistep development of human tumors with the unique feature of genomic instability(Shen,2011).These cancer characteristics include sustaining proliferative signaling,evading growth suppressors,resisting cell death,enabling replicative immortality,inducing angiogenesis,and activating invasion and metastasis(Chen et al.,2011;Song et al.,2018).Triple-negative breast cancer(TNBC),an aggressive disease with increased risks for visceral metastases,has a poor prognosis due to unavailable and viable therapeutic targets(Bianchini et al.,2016).A TNBC diagnosis indicates that cancer cells test negative for three key receptors:estrogen receptor,progesterone receptor,and human epidermal growth factor receptor 2(Bianchini et al.,2016).The absence of these three receptors renders existing hormone and targeted therapies ineffective. | McKay Mullen Fengrui Yang Jun Cao Yang Cao Xu Liu Gee Young Lee Tao Li William Yao Zhihong Yang Jiahai Zhang Kela Johnson Felix Aikhionbare Yong Chen Xinjiao Gao Dongmei Wang Xia Ding Hadiyah-Nicole Green Xing Liu Xuebiao Yao | 2021 | Journal of Molecular Cell Biology2021，13，11： | 0 |
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