Sharing data - p1273

doi:10.1038/ncb1109-1273a

Reference datasets should be accessible independently of scientific papers in a citable form, allowing attribution.

Full Text - Sharing data | PDF (115 KB) - Sharing data

Funding pain in Spain - p1273

doi:10.1038/ncb1109-1273b

On the eve of budget decisions, the scale of cuts to basic research funding remains ill-defined.

Full Text - Funding pain in Spain | PDF (115 KB) - Funding pain in Spain

Change is good: life outside the nucleus - p1274

Randy Schekman

doi:10.1038/ncb1109-1274

Full Text - Change is good: life outside the nucleus | PDF (93 KB) - Change is good: life outside the nucleus

Cyclin-dependent kinases: a family portrait - pp1275 - 1276

Marcos Malumbres, Edward Harlow, Tim Hunt, Tony Hunter, Jill M. Lahti, Gerard Manning, David O. Morgan, Li-Huei Tsai & Debra J. Wolgemuth

doi:10.1038/ncb1109-1275

Full Text - Cyclin-dependent kinases: a family portrait | PDF (179 KB) - Cyclin-dependent kinases: a family portrait | Supplementary information

Spermidine surprise for a long life - pp1277 - 1278

Matt Kaeberlein

doi:10.1038/ncb1109-1277

Identifying therapies to slow down ageing and delay age-associated diseases is a primary goal of ageing-related research. Resveratrol and rapamycin were first found to promote longevity in yeast, and their effects were then extended to several organisms. Spermidine is a new longevity drug that can increase life span in yeast, nematodes and flies, possibly through an effect on chromatin-mediated regulation of gene expression.

Full Text - Spermidine surprise for a long life | PDF (168 KB) - Spermidine surprise for a long life

See also: Article by Eisenberg et al.

Tip60-ing the balance in DSB repair - pp1279 - 1281

Wolfgang Fischle

doi:10.1038/ncb1109-1279

The tumour suppressor Tip60 is a histone acetyltransferase implicated in transcriptional control and DNA double-strand break repair. Tip60 binds to the heterochromatic histone mark H3K9me3, triggering acetylation and activation of DNA double-strand break repair factors.

Full Text - Tip60-ing the balance in DSB repair | PDF (312 KB) - Tip60-ing the balance in DSB repair

See also: Letter by Sun et al.

TGF- helps cells fly solo - pp1281 - 1284

Lauren A. Matise, Michael W. Pickup & Harold L. Moses

doi:10.1038/ncb1109-1281

Intravital imaging demonstrates that TGF- signalling regulates the mode of cancer cell motility. Cells with active TGF- signalling migrate as single cells and are capable of hematogenous and lymphatic spread, whereas cells lacking TGF- signalling invade lymphatics collectively.

Full Text - TGF- helps cells fly solo | PDF (2,436 KB) - TGF- helps cells fly solo

See also: Article by Giampieri et al.

Research highlights - p1285

Nathalie Le Bot, Silvia Grisendi, Christina Karlsson Rosenthal & Sowmya Swaminathan

doi:10.1038/ncb1109-1285

Full Text - Research highlights | PDF (95 KB) - Research highlights

Localized and reversible TGF signalling switches breast cancer cells from cohesive to single cell motility - pp1287 - 1296

Silvia Giampieri, Cerys Manning, Steven Hooper, Louise Jones, Caroline S. Hill & Erik Sahai

doi:10.1038/ncb1973

In vivo imaging of mammary carcinoma cells reveals that activation of a TGF-induced transcriptional response induces the motility of individual cells, allowing them to spread through the blood stream. In the absence of TGF, cells migrate as groups and can only metastasize through the lymphatic system.

Abstract - Localized and reversible TGF[beta] signalling switches breast cancer cells from cohesive to single cell motility | Full Text - Localized and reversible TGF signalling switches breast cancer cells from cohesive to single cell motility | PDF (4,460 KB) - Localized and reversible TGF signalling switches breast cancer cells from cohesive to single cell motility | Supplementary information

See also: News and Views by Matise et al.

KLF17 is a negative regulator of epithelial–mesenchymal transition and metastasis in breast cancer - pp1297 - 1304

Kiranmai Gumireddy, Anping Li, Phyllis A. Gimotty, Andres J. Klein-Szanto, Louise C. Showe, Dionyssios Katsaros, George Coukos, Lin Zhang & Qihong Huang

doi:10.1038/ncb1974

A screen for suppressors of breast to lung metastasis leads to the identification of KLF17 (Krüppel-like transcription factor 17), which is shown to be downregulated in breast cancer biopsies. KLF17 inhibits epithelial–mesenchymal transition and invasion by inhibiting the transcription of the metastasis factor Id1.

Abstract - KLF17 is a negative regulator of epithelial-mesenchymal transition and metastasis in breast cancer | Full Text - KLF17 is a negative regulator of epithelial–mesenchymal transition and metastasis in breast cancer | PDF (2,537 KB) - KLF17 is a negative regulator of epithelial–mesenchymal transition and metastasis in breast cancer | Supplementary information

Induction of autophagy by spermidine promotes longevity - pp1305 - 1314

Tobias Eisenberg, Heide Knauer, Alexandra Schauer, Sabrina Büttner, Christoph Ruckenstuhl, Didac Carmona-Gutierrez, Julia Ring, Sabrina Schroeder, Christoph Magnes, Lucia Antonacci, Heike Fussi, Luiza Deszcz, Regina Hartl, Elisabeth Schraml, Alfredo Criollo, Evgenia Megalou, Daniela Weiskopf, Peter Laun, Gino Heeren, Michael Breitenbach, Beatrix Grubeck-Loebenstein, Eva Herker, Birthe Fahrenkrog, Kai-Uwe Fröhlich, Frank Sinner, Nektarios Tavernarakis, Nadege Minois, Guido Kroemer & Frank Madeo

doi:10.1038/ncb1975

Administration of spermidine, a polyamine whose concentration declines during ageing, extends lifespan in yeast, flies, worms and in human immune cells. Spermidine prevents early oxidative stress and necrotic cell death and increases the expression of autophagy genes by inhibiting histone acetyltransferases action on histone H3.

Abstract - Induction of autophagy by spermidine promotes longevity | Full Text - Induction of autophagy by spermidine promotes longevity | PDF (3,106 KB) - Induction of autophagy by spermidine promotes longevity | Supplementary information

See also: News and Views by Kaeberlein

Topoisomerase I suppresses genomic instability by preventing interference between replication and transcription - pp1315 - 1324

Sandie Tuduri, Laure Crabbé, Chiara Conti, Hélène Tourrière, Heidi Holtgreve-Grez, Anna Jauch, Véronique Pantesco, John De Vos, Aubin Thomas, Charles Theillet, Yves Pommier, Jamal Tazi, Arnaud Coquelle & Philippe Pasero

doi:10.1038/ncb1984

Topoisomerase I, together with the splicing factor ASF/SF2, prevents the collapse of replication forks by inhibiting the formation of RNA–DNA hybrids during the transcription of genes localized at replicating forks, and thereby suppresses the genomic instability associated with such hybrids.

Abstract - Topoisomerase I suppresses genomic instability by preventing interference between replication and transcription | Full Text - Topoisomerase I suppresses genomic instability by preventing interference between replication and transcription | PDF (2,231 KB) - Topoisomerase I suppresses genomic instability by preventing interference between replication and transcription | Supplementary information

Slit2–Robo4 signalling promotes vascular stability by blocking Arf6 activity - pp1325 - 1331

Christopher A. Jones, Naoyuki Nishiya, Nyall R. London, Weiquan Zhu, Lise K. Sorensen, Aubrey C. Chan, Chinten J. Lim, Haoyu Chen, Qisheng Zhang, Peter G. Schultz, Alaa M. Hayallah, Kirk R. Thomas, Michael Famulok, Kang Zhang, Mark H. Ginsberg & Dean Y. Li

doi:10.1038/ncb1976

The Slit2 receptor Robo4 is known to maintain vascular permeability. Robo 4 prevents the formation of endothelial cell protrusions through a complex with paxillin and Arf–GAPs, which inhibits the GTPase Arf6a and thus leads to Rac activation.

First Paragraph - Slit2-Robo4 signalling promotes vascular stability by blocking Arf6 activity | Full Text - Slit2–Robo4 signalling promotes vascular stability by blocking Arf6 activity | PDF (1,961 KB) - Slit2–Robo4 signalling promotes vascular stability by blocking Arf6 activity | Supplementary information

Intraflagellar transport is required for polarized recycling of the TCR/CD3 complex to the immune synapse - pp1332 - 1339

Francesca Finetti, Silvia Rossi Paccani, Maria Giovanna Riparbelli, Emiliana Giacomello, Giuseppe Perinetti, Gregory J. Pazour, Joel L. Rosenbaum & Cosima T. Baldari

doi:10.1038/ncb1977

IFT20, known to control intraflagellar transport during cilia biogenesis, is also expressed in lymphoid and myeloid non-ciliated cells. IFT20 is localized to the secretory pathway in T-lymphocytes and translocates to the immune synapse on antigen engagement to modulate the recycling of T-cell receptors.

First Paragraph - Intraflagellar transport is required for polarized recycling of the TCR/CD3 complex to the immune synapse | Full Text - Intraflagellar transport is required for polarized recycling of the TCR/CD3 complex to the immune synapse | PDF (3,658 KB) - Intraflagellar transport is required for polarized recycling of the TCR/CD3 complex to the immune synapse | Supplementary information

Analysis of the -secretase interactome and validation of its association with tetraspanin-enriched microdomains - pp1340 - 1346

Tomoko Wakabayashi, Katleen Craessaerts, Leen Bammens, Mostafa Bentahir, Filip Borgions, Piet Herdewijn, An Staes, Evy Timmerman, Joël Vandekerckhove, Eric Rubinstein, Claude Boucheix, Kris Gevaert & Bart De Strooper

doi:10.1038/ncb1978

The -secretase complex is responsible for the generation of amyloid -peptide, the main component of Alzheimer's disease associated plaques. A proteomic analysis yielded secretory pathway components and membrane-associated tetraspannin microdomains as interactors and regulators of the -secretase complex.

First Paragraph - Analysis of the [gamma]-secretase interactome and validation of its association with tetraspanin-enriched microdomains | Full Text - Analysis of the -secretase interactome and validation of its association with tetraspanin-enriched microdomains | PDF (2,383 KB) - Analysis of the -secretase interactome and validation of its association with tetraspanin-enriched microdomains | Supplementary information

Tudor staphylococcal nuclease is an evolutionarily conserved component of the programmed cell death degradome - pp1347 - 1354

Jens F. Sundström, Alena Vaculova, Andrei P. Smertenko, Eugene I. Savenkov, Anna Golovko, Elena Minina, Budhi S. Tiwari, Salvador Rodriguez-Nieto, Andrey A. Zamyatnin, Jr, Tuuli Välineva, Juha Saarikettu, Mikko J. Frilander, Maria F. Suarez, Anton Zavialov, Ulf Ståhl, Patrick J. Hussey, Olli Silvennoinen, Eva Sundberg, Boris Zhivotovsky & Peter V. Bozhkov

doi:10.1038/ncb1979

Substrates of plant metacaspases, cystein proteases involved in plant programmed cell death (PCD), have been so far unknown. Metacaspase II is now shown to cleave the splicing regulator Tudor staphylococcal nuclease (TSN) during developmental and stress-induced PCD, an activity shared with caspase-3 during apoptosis in animals.

First Paragraph - Tudor staphylococcal nuclease is an evolutionarily conserved component of the programmed cell death degradome | Full Text - Tudor staphylococcal nuclease is an evolutionarily conserved component of the programmed cell death degradome | PDF (2,901 KB) - Tudor staphylococcal nuclease is an evolutionarily conserved component of the programmed cell death degradome | Supplementary information

FLIP-mediated autophagy regulation in cell death control - pp1355 - 1362

Jong-Soo Lee, Qinglin Li, June-Yong Lee, Sun-Hwa Lee, Joseph H. Jeong, Hye-Ra Lee, Heesoon Chang, Fu-Chun Zhou, Shou-Jiang Gao, Chengyu Liang & Jae U. Jung

doi:10.1038/ncb1980

Two inhibitors of death receptor-associated apoptosis, cellular c-FLIP and viral v-FLIP prevents LC3 processing by Atg3 and thus repress the autophagic cell death that follows mTOR inhibition. Short peptides derived from FLIP can prevent Atg3–FLIP interaction without affecting Atg3–LC3, restoring cell death.

First Paragraph - FLIP-mediated autophagy regulation in cell death control | Full Text - FLIP-mediated autophagy regulation in cell death control | PDF (5,286 KB) - FLIP-mediated autophagy regulation in cell death control | Supplementary information

UBE2S elongates ubiquitin chains on APC/C substrates to promote mitotic exit - pp1363 - 1369

Mathew J. Garnett, Jörg Mansfeld, Colin Godwin, Takahiro Matsusaka, Jiahua Wu, Paul Russell, Jonathon Pines & Ashok R. Venkitaraman

doi:10.1038/ncb1983

The anaphase-promoting complex (APC/C), a ubiquitin ligase regulating mitotic progression, is a target for spindle assembly checkpoint. UBE2S, an ubiquitin-conjugating enzyme, is identified as a novel factor that elongates ubiquitin chains and promotes APC/C substrate degradation following release from the spindle assembly checkpoint.

First Paragraph - UBE2S elongates ubiquitin chains on APC/C substrates to promote mitotic exit | Full Text - UBE2S elongates ubiquitin chains on APC/C substrates to promote mitotic exit | PDF (1,967 KB) - UBE2S elongates ubiquitin chains on APC/C substrates to promote mitotic exit | Supplementary information

Transcriptional repression of p53 by parkin and impairment by mutations associated with autosomal recessive juvenile Parkinson's disease - pp1370 - 1375

Cristine Alves da Costa, Claire Sunyach, Emilie Giaime, Andrew West, Olga Corti, Alexis Brice, Stephen Safe, Patrick M. Abou-Sleiman, Nicholas W. Wood, Hitoshi Takahashi, Mathew S. Goldberg, Jie Shen & Frédéric Checler

doi:10.1038/ncb1981

Parkin, an ubiquitin ligase whose mutations are associated with early development of Parkinson's disease, possesses a RING domain, suggesting it can modulate transcription. Parkin represses the expression of p53 both in fibroblasts and mice brains, independently of its ligase activity, and patient brain samples exhibit high levels of p53.

First Paragraph - Transcriptional repression of p53 by parkin and impairment by mutations associated with autosomal recessive juvenile Parkinson's disease | Full Text - Transcriptional repression of p53 by parkin and impairment by mutations associated with autosomal recessive juvenile Parkinson's disease | PDF (1,635 KB) - Transcriptional repression of p53 by parkin and impairment by mutations associated with autosomal recessive juvenile Parkinson's disease | Supplementary information

Histone H3 methylation links DNA damage detection to activation of the tumour suppressor Tip60 - pp1376 - 1382

Yingli Sun, Xiaofeng Jiang, Ye Xu, Marina K. Ayrapetov, Lisa A. Moreau, Johnathan R. Whetstine & Brendan D. Price

doi:10.1038/ncb1982

Tip60 acetylation of ATM kinase is necessary for DNA double-strand break repair and cancer suppression. Tip60 is recruited to breaks by histoneH3 trimethylated on lysine 9 and the Mre11/Rad50/Nbs1 damage response complex, activating its acetyltransferase activity.

First Paragraph - Histone H3 methylation links DNA damage detection to activation of the tumour suppressor Tip60 | Full Text - Histone H3 methylation links DNA damage detection to activation of the tumour suppressor Tip60 | PDF (2,291 KB) - Histone H3 methylation links DNA damage detection to activation of the tumour suppressor Tip60 | Supplementary information

See also: News and Views by Fischle

DNA damage signalling prevents deleterious telomere addition at DNA breaks - pp1383 - 1386

Svetlana Makovets & Elizabeth H. Blackburn

doi:10.1038/ncb1985

The enzyme telomerase extends telomeres at unprotected chromosomal ends. DNA double-stranded breaks could also form a substrate for telomerase, but DNA damage signalling induces the phosphorylation of the telomerase inhibitor Pif1 at breaks, preventing ectopic addition of telomeres at sites of repair and hence genomic instability.

Abstract - DNA damage signalling prevents deleterious telomere addition at DNA breaks | Full Text - DNA damage signalling prevents deleterious telomere addition at DNA breaks | PDF (1,166 KB) - DNA damage signalling prevents deleterious telomere addition at DNA breaks | Supplementary information

Functional interaction between FOXO3a and ATM regulates DNA damage response - p1387

Wen-Bin Tsai, Young Min Chung, Yoko Takahashi, Zhaohui Xu & Mickey C-T. Hu

doi:10.1038/ncb1109-1387a

Full Text - Functional interaction between FOXO3a and ATM regulates DNA damage response | PDF (219 KB) - Functional interaction between FOXO3a and ATM regulates DNA damage response

Oxidant-induced apoptosis is mediated by oxidation of the actin-regulatory protein cofilin - p1387

Fábio Klamt, Stéphanie Zdanov, Rodney L. Levine, Ashley Pariser, Yaqin Zhang, Baolin Zhang, Li-Rong Yu, Timothy D. Veenstra & Emily Shacter

doi:10.1038/ncb1109-1387b

Full Text - Oxidant-induced apoptosis is mediated by oxidation of the actin-regulatory protein cofilin | PDF (219 KB) - Oxidant-induced apoptosis is mediated by oxidation of the actin-regulatory protein cofilin

MyosinV controls PTEN function and neuronal cell size - p1387

Michiel T. van Diepen, Maddy Parsons, C. Peter Downes, Nicholas R. Leslie, Robert Hindges & Britta J Eickholt

doi:10.1038/ncb1109-1387c

Full Text - MyosinV controls PTEN function and neuronal cell size | PDF (219 KB) - MyosinV controls PTEN function and neuronal cell size