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From our sister journals- January 2016

Posted by , on 26 January 2016

Here is some developmental biology-related content from other journals published by The Company of Biologists.




Characterisation of Slc9a6 knockout heterozygous female mice

DMM Jan2016Mutations in SLC9A6 are responsible for X-linked Christianson syndrome, a neurodevelopmental disease. Sikora and colleagues demonstrate that female mice heterozygous for a Slc9a6 knockout present mosaic neuropathology and similar but milder behavioural traits to those of affected males. Read the paper here. [OPEN ACCESS]




Journal typography


Sp5 emerges as an important component in mESC naïve pluripotency

JCSJan2016_1Sp5 has been identified as an effector of both Wnt/β-catenin and leukemia inhibitory factor (LIF)/Stat3 pluripotency signaling, and its forced expression produces effects of both pathways in mESC pluripotency. Furthermore, Sp5 can convert mouse epiblast stem cells into mESCs. Read the paper here. [OPEN ACCESS]



FGF signalling on E-Cadherin impacts primordial germ cell motility

JCSJan2016_2In this paper, Parès and Ricardo describe how fibroblast growth factor (FGF) signaling modulates zygotic E-cadherin distribution to maintain posterior midgut epithelial 3D architecture, impacting on primordial germ cell motility during the early embryonic development of Drosophila. Read the paper here.



Targets identified for NF-κB-modulated microRNAs that inhibit myoblast proliferation

JCSJan2016_3Wei and colleagues show that miR-195 and miR-497 target lgf1rlnsrCcnd2 and Ccne1 and inhibit proliferation in C2C12 cells. They also show that these microRNAs are negatively regulated by nuclear factor κB, illustrating an important signalling pathway in myogenesis. Read the paper here.



Reciprocal regulation of alternative lineages by Rgs18 and its transcriptional repressor Gfi1b

JCSJan2016_4Sengupta and colleagues describe how Rgs18, a GTPase-activating protein, and its transcriptional repressor Gfi1b reciprocally regulate the lineage segregation between the megakaryocytic and the erythroid lineage through the downstream effects on the antagonistic transcription factors Fli1 and Klf1. Read the paper here.




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