A serine/threonine kinase gene defective in Peutz–Jeghers syndrome

Nature ◽  
10.1038/34432 ◽  
1998 ◽  
Vol 391 (6663) ◽  
pp. 184-187 ◽  
Author(s):  
Akseli Hemminki ◽  
David Markie ◽  
Ian Tomlinson ◽  
Egle Avizienyte ◽  
Stina Roth ◽  
...  
2004 ◽  
Vol 35 (6) ◽  
pp. 497-497 ◽  
Author(s):  
J. Meyer ◽  
H. Murua Escobar ◽  
S. Bartnitzke ◽  
C. Schelling ◽  
G. Dolf ◽  
...  

1999 ◽  
Vol 262 (2) ◽  
pp. 456-466 ◽  
Author(s):  
Colin N. MacDougall ◽  
Dorothy Clyde ◽  
Timothy Wood ◽  
Martin Todman ◽  
Diane Harbison ◽  
...  

2007 ◽  
Vol 6 (6) ◽  
pp. 997-1005 ◽  
Author(s):  
Xiao-Hong Liu ◽  
Jian-Ping Lu ◽  
Lei Zhang ◽  
Bo Dong ◽  
Hang Min ◽  
...  

ABSTRACT We isolated an MgATG1 gene encoding a serine/threonine protein kinase from the rice blast fungus Magnaporthe grisea. In the ΔMgatg1 mutant, in which the MgATG1 gene had been deleted, autophagy was blocked; the mutant also showed fewer lipid droplets in its conidia, lower turgor pressure of the appressorium, and such defects in morphogenesis as delayed initiation and slower germination of conidia. As a result of lower turgor pressure of the appressorium, the ΔMgatg1 mutant lost its ability to penetrate and infect the two host plants, namely, rice and barley. However, normal values of the parameters and infective abilities were restored on reintroducing an intact copy of the MgATG1 gene into the mutant. Autophagy is thus necessary for turnover of organic matter during the formation of conidia and appressoria and for normal development and pathogenicity in M. grisea.


2014 ◽  
Vol 207 (2) ◽  
pp. 299-315 ◽  
Author(s):  
Keefe T. Chan ◽  
Sreeja B. Asokan ◽  
Samantha J. King ◽  
Tao Bo ◽  
Evan S. Dubose ◽  
...  

Somatic inactivation of the serine/threonine kinase gene STK11/LKB1/PAR-4 occurs in a variety of cancers, including ∼10% of melanoma. However, how the loss of LKB1 activity facilitates melanoma invasion and metastasis remains poorly understood. In LKB1-null cells derived from an autochthonous murine model of melanoma with activated Kras and Lkb1 loss and matched reconstituted controls, we have investigated the mechanism by which LKB1 loss increases melanoma invasive motility. Using a microfluidic gradient chamber system and time-lapse microscopy, in this paper, we uncover a new function for LKB1 as a directional migration sensor of gradients of extracellular matrix (haptotaxis) but not soluble growth factor cues (chemotaxis). Systematic perturbation of known LKB1 effectors demonstrated that this response does not require canonical adenosine monophosphate–activated protein kinase (AMPK) activity but instead requires the activity of the AMPK-related microtubule affinity-regulating kinase (MARK)/PAR-1 family kinases. Inhibition of the LKB1–MARK pathway facilitated invasive motility, suggesting that loss of the ability to sense inhibitory matrix cues may promote melanoma invasion.


Development ◽  
2000 ◽  
Vol 127 (7) ◽  
pp. 1467-1475 ◽  
Author(s):  
J.L. Watts ◽  
D.G. Morton ◽  
J. Bestman ◽  
K.J. Kemphues

During the first cell cycle of Caenorhabditis elegans embryogenesis, asymmetries are established that are essential for determining the subsequent developmental fates of the daughter cells. The maternally expressed par genes are required for establishing this polarity. The products of several of the par genes have been found to be themselves asymmetrically distributed in the first cell cycle. We have identified the par-4 gene of C. elegans, and find that it encodes a putative serine-threonine kinase with similarity to a human kinase associated with Peutz-Jeghers Syndrome, LKB1 (STK11), and a Xenopus egg and embryo kinase, XEEK1. Several strong par-4 mutant alleles are missense mutations that alter conserved residues within the kinase domain, suggesting that kinase activity is essential for PAR-4 function. We find that the PAR-4 protein is present in the gonads, oocytes and early embryos of C. elegans, and is both cytoplasmically and cortically distributed. The cortical distribution begins at the late 1-cell stage, is more pronounced at the 2- and 4-cell stages and is reduced at late stages of embryonic development. We find no asymmetry in the distribution of PAR-4 protein in C. elegans embryos. The distribution of PAR-4 protein in early embryos is unaffected by mutations in the other par genes.


Author(s):  
Wilfried Reichardt ◽  
Volker Jung ◽  
Christian Brunner ◽  
Alexandra Klein ◽  
Silke Wemmert ◽  
...  

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