ライフサイエンスコーパス: crossvein

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1 g differentiation of cells into the anterior crossvein.

2 is downregulated in the developing posterior crossvein.

3 of longitudinal wing vein 4 and the anterior crossvein.

4 ed for the promotion of BMP signaling in the crossveins.

5 ring' of the wing and the formation of extra crossveins.

6 and in the correct positioning of veins and crossveins.

7 f phosphorylated Mad and dSRF in presumptive crossvein cells.

8 n (Dg) are similarly viable and exhibit this crossvein defect, indicating that both of the central DA

9 Second, BMP signaling in the posterior crossvein depends on Decapentaplegic (Dpp) at a stage wh

10 We find that loss or gain of kek5 disrupts crossvein development and alters the early profile of ph

11 First, the initial stage of posterior crossvein development depends on BMP signaling but is in

12 t this prepattern is essential for posterior crossvein development.

13 The initial specification of crossvein fate in the Drosophila wing requires signaling

14 Large sog clones disrupt posterior crossvein formation, suggesting that Sog and Cv act toge

15 ere that a similar mechanism operates during crossvein formation, utilizing Sog and a new member of t

16 ins, and this results in the production of a crossvein fragment in the intervein between the two long

17 The sensitivity of the posterior crossvein in the pupal wing of Drosophila to reductions

18 fects, including the formation of an ectopic crossvein in the wing, but they have a short lifespan.

19 nes for association with the location of the crossveins in the central region of the wing.

20 ning of appendages, including the spacing of crossveins in the wing and the segmentation of the leg t

21 ling during the development of the posterior crossvein, mutate a lipoprotein that is similar to the v

22 The sensitivity of the crossveins of the Drosophila wing to reductions in BMP s

23 and Tld during development of the posterior crossvein (PCV) in the pupal wing.

24 We also found that the ectopic crossvein phenotype can be induced by expression of a mu

25 sses dSRF levels in the neighboring anterior crossvein progenitor cells, allowing them to differentia

26 rodimer from the longitudinal veins into the crossvein regions.

27 ngs, the early BMP signalling that initiates crossvein specification is not maintained, particularly

28 locus is the variable loss of the posterior crossvein that has been described for alleles of det.

29 Thus, the posterior crossvein will be especially vulnerable to reductions in

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