Papers Selected in 2013 (Jan.-July)

Long-term treatment with metformin starting at middle age extends healthspan and lifespan in male mice.

  SUMOylation (SUMO, small ubiquitin-like modifier) of PTEN controls its nuclear localization. See the Perspective by Leslie and Brunton.

Hours before it dies, a wave of blue fluorescence flows through the body of C. elegans.

A behavioral database for Caenorhabditis elegans strains. The database also has short videos that display behavior and morphology features.

 PTEN mediates chemorepulsion in growing axons.

Phosphorylated PTEN relative to its unphosphorylated counterpart shows reduced catalytic activity and membrane affinity and undergoes conformational compaction likely involving an intramolecular interaction between its C-tail and the C2 domain.

 Andrew Chisholm's review on cytoskeleton dynamics in axon regeneration.

a href="">  EGL-18 and ELT-6  are  needed for seam cell fate during embryogenesis, are reused downstream of Wnt signaling in the maintenance of seam cell fates during the larval asymmetric stem cell-like divisions.

a negative feedback loop between the C. elegans detoxification/antioxidant response factor SKN-1/Nrf and its repressor wdr-23

Protein kinase A (PKA) stabilizes active wakefulness, at least in part through two of its downstream targets: neuropeptide release and CREB

  Biotechniques has a profile on Cori Bargmann.

CRISPR-Cas9 system for generating loss-of-function mutants in C. elegans. See  this paper too:

Dan Dickinson and Bob Goldstein run a website for information on Cas9 recombination in C. elegans.

See this commentary from Christian Frøkjær-Jensen . 

 New wormbook chapter on transcriptional regulation in C. elegans.

A library of 2,007 mutagenized C. elegans strains, with mutant alleles for each of the worm's more than 20,000 genes. The library contains over 800,000 unique single nucleotide changes.

Review on L1 arrest.

  PTEN-Long is a membrane permeable lipid phosphatase that is secreted from cells and can enter other cells. Also see this perspective and paper on intracellular PTEN.

 When fed the soil bacteria Comamonas, C. elegans develop faster, lay fewer eggs, and live shorter than when fed E. coli  OP50. Mixing of food experiments show that Comamonas DA1877 effect is “dominant” over that of E. coli OP50 . See this paper too:  

Forward and reverse genetic screens uncover diet-response network in C. elegans ► Mutations in human orthologs cause inborn metabolic disorders treated by diet ► Mitochondrial metabolic and nuclear regulatory networks communicate reciprocally ► Multiple transcription factors mediate the metabolic network perturbation response

AMPK contributes to survival during L1 diapause in a manner distinct from that by which it controls dauer diapause.  AMPK suppresses TORC1 activity to maintain stem cell quiescence but TORC1 activity appears to function independently for L1 diapause longevity.   

Novel lipid-TORC1 signaling pathway that coordinates nutrient and metabolic status with post embryonic growth.  See also this paper.

The tumor suppressor Rb and cell metabolism.  Dispatch for the paper below:

 Rb plays critical roles in promoting L1 starvation survival and function in both IIS-dependent and -independent pathways. 

 How can a cell control how big it is?


 New mechanisms that rely less on actomyosin contractility of purse-string bundles and more on dynamics in the global cortical actomyosin network of the cells. 

 Zou et al. report that the highly conserved let-7–LIN-41 heterochronic signaling pathway is responsible for part of the age-related decline in axon regeneration in the worm Caenorhabditis elegans.

 Understanding PTEN regulation may help us better interpret tumour development. Also see this review on non-genomic loss of PTEN function.

 Genetic similarities between sleep regulation during C. elegans lethargus and sleep regulation in other animals.

LAR modulates cell migration through EphA2 site-specific dephosphorylation

 Worms deprived of sleep die.  daf-16 mutants show an  are hypersensitive to the lethal effects of forced locomotion during lethargus.

This review describes several target sites that could help in the development of novel drug candidates to regulate or restore the normal physiological functions of PTEN and are essential in the treatment of human diseases where PTEN plays a pivotal role.


 Kinesin-2 motors mediate anterograde intraflagellar transport (IFT).  Bardet-Biedl syndrome (BBS) and IFT-A proteins are now implicated in regulation of IFT assembly at the ciliary base and tip.

EphA2 is expressed in human thyroid cancer. Phosphorylated Akt (pAkt), an important regulator of thyroid cancer metastasis, is attenuated by EphA2 knockdown, providing evidence that EphA2 may act through pAkt. Matrigel invasion of thyroid cancer cell lines correlates with EphA2 expression and loss of PTEN. This is consistent with what is seen in 

C. elegan  Eph and PTEN regulation.


 Axon tracts are critical for patterning the C. elegans body. The CAN neurons express the Ror family wnt receptor which "soaks" up wnt ligands in the posterior end. In vab-8 mutants the CAN cell body and posterior axons are anteriorly displaced leading to more wnts in the posterior end which induces ectopic  vulval cells in the posterior end. 

 Down regulation of the Insulin/IGF-1-like signaling (IIS) pathway protects neurons from degenerating in a DAF-16/FOXO-dependent manner and is related to superoxide dismutase and catalase-increased expression.

 Handedness in the worm is independent of body symmetry and may be is driven by epigenetic factors rather than by genetic variation.

 Protocol for C. elegans triple-fluorescence imaging approach for time-lapse imaging analysis such as Q neuroblast migration in the L1 larvae. 

 New mechanistic insights about the role of PTEN in metabolism.

 A method to express active ephrin in  bacteria. 

 Latest review on PTEN