C. elegans serine-threonine kinase KIN-29 modulates TGFβ signaling and regulates body size formationReportar como inadecuado

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BMC Developmental Biology

, 5:8

First Online: 19 April 2005Received: 19 November 2004Accepted: 19 April 2005 Background

In C. elegans there are two well-defined TGFβ-like signaling pathways. The Sma-Mab pathway affects body size morphogenesis, male tail development and spicule formation while the Daf pathway regulates entry into and exit out of the dauer state. To identify additional factors that modulate TGFβ signaling in the Sma-Mab pathway, we have undertaken a genetic screen for small animals and have identified kin-29.

Resultskin-29 encodes a protein with a cytoplasmic serine-threonine kinase and a novel C-terminal domain. The kinase domain is a distantly related member of the EMK ELKL motif kinase family, which interacts with microtubules. We show that the serine-threonine kinase domain has in vitro activity. kin-29 mutations result in small animals, but do not affect male tail morphology as do several of the Sma-Mab signal transducers. Adult worms are smaller than the wild-type, but also develop more slowly. Rescue by kin-29 is achieved by expression in neurons or in the hypodermis. Interaction with the dauer pathway is observed in double mutant combinations, which have been seen with Sma-Mab pathway mutants. We show that kin-29 is epistatic to the ligand dbl-1, and lies upstream of the Sma-Mab pathway target gene, lon-1.

Conclusionkin-29 is a new modulator of the Sma-Mab pathway. It functions in neurons and in the hypodermis to regulate body size, but does not affect all TGFβ outputs, such as tail morphogenesis.

Electronic supplementary materialThe online version of this article doi:10.1186-1471-213X-5-8 contains supplementary material, which is available to authorized users.

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Autor: Lisa L Maduzia - Andrew F Roberts - Huang Wang - Xia Lin - Lena J Chin - Cole M Zimmerman - Stephen Cohen - Xin-Hua Fe

Fuente: https://link.springer.com/article/10.1186/1471-213X-5-8

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