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In Focus

Loss of protein from neighbors tells migrating cells they are in the vanguard.

People & Ideas

Welch investigates how host cells and pathogens initiate actin polymerization.



Phosphorylation of Polη links DNA damage–induced checkpoint activation and translesion synthesis in mammalian cells.

While ESCRT-0 is ubiquitinated by the Rsp5 E3 ligase, loss of Rsp5 does not disrupt monoubiquitin-dependent sorting into multivesicular bodies.

N-WASP–deficient Schwann cells sort and ensheath axons but arrest at the promyelinating stage.


The single-strand DNA–binding protein RPA promotes 5′-strand resection to generate 3′ single strands for homology-dependent DNA double-strand repair.

The meiosis-specific kleisin cohesin subunit, RAD21L, may participate in synapsis initiation and crossover recombination between homologous chromosomes.

The Pol I subunits Rpa34 and Rpa49, required for elongation and 35S rRNA production, promote clustering of neighboring Pol I complexes to enhance the rRNA gene transcription cycle.

The ubiquitin hydrolase activating factor Bro1 enhances ESCRT-III stability by inhibiting Vps4-mediated disassembly.

Formation of actin-rich structures along the lateral borders of subperineurial glial cells are induced and maintained by the G protein–coupled receptor Moody.

The compliance and dimensionality of the ECM regulate distinct changes in microtubule growth speed and growth persistence.

Upon loss of a binding partner in apposed tissue, the homophilic cell adhesion protein Echinoid adopts a planar polarized localization, which promotes the planar polarized localization of the planar cell polarity protein Bazooka/Par-3 and targets actomyosin cable assembly to the epidermal leading edge, thus establishing the migration direction of the developing epidermis.

The dystrophin protein complex, an important regulator of muscle membrane integrity, also maintains neural organization through interactions with the L1CAM family member SAX-7.


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