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UniProt release 2019_02

新疆十一选五开奖结果 www.6nbnc.cn Published February 13, 2019

Headline

Let’s twist again with Myo1D

At first glance, we look bilaterally symmetrical. Our left side appears pretty much the mirror image of the right one. For our internal organs, it’s a completely different story. For instance, our heart is on the left of our body, while the liver lies to the right. Macroscopic left-right patterning is only one aspect of an organism’s asymmetry. Actually all known life forms show asymmetric properties in chemical structures, as well as in macroscopic anatomy, development and behavior. However, not much is known about the nature of the link between molecular-level and macroscopic asymmetry.

Studies in Drosophila led to the discovery of a crucial role for an unconventional myosin, called Myo31DF or Myo1D, in left-right asymmetry. Myo1D inactivation in the fly can reverse handedness of the gut and testes. In a recent publication, Lebreton et al. have extended these observations, showing that ectopic expression of Myo1D in ‘naive’ tissues, i.e. devoid of left-right asymmetry, such as epidermis and trachea, was sufficient to drive laterality. In the larval epidermis, Myo1D expression induced dextral twisting of the whole larval body, which could rotate up to 180°, resulting in abnormal crawling behavior. In the trachea, pronounced right-handed twisting, with a spiraling ribbon shape with multiple turns, was observed instead of the smooth and linear conformation of the wild-type tissue. This asymmetry was also seen at the cellular level. In control conditions, epidermal cells were perpendicular to the anterior-posterior axis. In contrast, cells ectopically expressing Myo1D showed elongation and a clear shift in membrane orientation toward one side. Myo1D functions as an actin-based motor protein with ATPase activity and this activity was required for the establishment of left-right asymmetry. In vitro Myo1D caused actin filaments to move in anticlockwise circular motion, suggesting that the multiscale property of Myo1D emerges from its molecular interaction with F-actin.

Does this conclusion apply to vertebrates? This answer is not straightforward. Experiments in some vertebrates point to a role for MYO1D in left-right patterning. In Xenopus, MYO1D morpholino knockdown affected organ placement in over 50% of the morphant tadpoles. In Zebrafish, MYO1D plays a role in the formation of Kupffer’s vesicle, an organ that functions as left-right organizer during embryogenesis. However, in rat, MYO1D knockout didn’t lead to visceral situs inversus and caused no obvious motor defects, indicating that, at least in certain mammals, MYO1D is not involved in left-right body asymmetry.

As of this release, UniProtKB/Swiss-Prot MYO1D entries have been updated and are publicly available.

UniProtKB news

Removal of the cross-references to CleanEx

Cross-references to CleanEx have been removed.

Changes to the controlled vocabulary of human diseases

New diseases:

Modified diseases:

Changes to the controlled vocabulary for PTMs

New term for the feature key ‘Modified residue’ (‘MOD_RES’ in the flat file):

  • ADP-ribosyldiphthamide

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Change of URIs for Orphanet

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The URIs for the Orphanet database have therefore been updated from:

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to:
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If required for backward compatibility, you can use the following query to add the old URIs:
PREFIX owl:<//www.w3.org/2002/07/owl#>
PREFIX up:<//purl.uniprot.org/core/>
INSERT
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   ?protein rdfs:seeAlso ?old .
   ?old owl:sameAs ?new .
   ?old up:database <//purl.uniprot.org/database/orphanet> .
}
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{
   ?protein rdfs:seeAlso ?new .
   ?new up:database <//purl.uniprot.org/database/Orphanet> .
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}

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