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Title: The Gaia -ESO Survey: Age spread in the star forming region NGC 6530 from the HR diagram and gravity indicators
Award ID(s):
1813881
NSF-PAR ID:
10098547
Author(s) / Creator(s):
; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; more » ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; « less
Date Published:
Journal Name:
Astronomy & Astrophysics
Volume:
623
ISSN:
0004-6361
Page Range / eLocation ID:
A159
Format(s):
Medium: X
Sponsoring Org:
National Science Foundation
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  1. Abstract Background

    Vertebrate eye formation requires coordinated inductive interactions between different embryonic tissue layers, first described in amphibians. A network of transcription factors and signaling molecules controls these steps, with mutations causing severe ocular, neuronal, and craniofacial defects. Ineyelessmutant axolotls, eye morphogenesis arrests at the optic vesicle stage, before lens induction, and development of ventral forebrain structures is disrupted.

    Results

    We identified a 5‐bp deletion in therax(retina and anterior neural fold homeobox) gene, which was tightly linked to the recessiveeyeless(e) axolotl locus in an F2 cross. This frameshift mutation, in exon 2, truncates RAX protein within the homeodomain (P154fs35X). Quantitative RNA analysis shows that mutant and wild‐typeraxtranscripts are equally abundant inE/eembryos. Translation appears to initiate from dual start codons, via leaky ribosome scanning, a conserved feature among gnathostome RAX proteins. Previous data showraxis expressed in the optic vesicle and diencephalon, deeply conserved among metazoans, and required for eye formation in other species.

    Conclusion

    Theeyelessaxolotl mutation is a null allele in theraxhomeobox gene, with primary defects in neural ectoderm, including the retinal and hypothalamic primordia.

     
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  2. ABSTRACT

    The XXL Survey is the largest homogeneous survey carried out with XMM-Newton. Covering an area of 50 deg2, the survey contains several hundred galaxy clusters out to a redshift of ≈2, above an X-ray flux limit of ∼6 × 10−15 er g cm−2 s−1. The GAMA spectroscopic survey of ∼300 000 galaxies covers ≈286 deg2, down to an r-band magnitude of r < 19.8 mag. The region of overlap of these two surveys (covering 14.6 deg2) represents an ideal opportunity to study clusters selected via two independent selection criteria. Generating two independently selected samples of clusters, one drawn from XXL (spanning a redshift range 0.05 ≤ z ≤ 0.3) and another from GAMA (0.05 ≤ z ≤ 0.2), both spanning 0.2 ≲ M500 ≲ 5 × 1014 M⊙, we investigate the relationship between X-ray luminosity and velocity dispersion (LX − σv relation). Comparing the LX − σv relation between the X-ray selected and optically selected samples, when not accounting for the X-ray selection, we find that the scatter of the X-ray selected sample is 2.7 times higher than the optically selected sample (at the 3.7σ level). Accounting for the X-ray selection to model the LX − σv relation, we find that the difference in the scatter increases (with the X-ray selected sample having a scatter 3.4 times larger than the optically selected sample). Although the scatter of the optically selected sample is lower, we find 13 optically selected GAMA groups undetected in X-rays. Inspection of the difference in magnitude between the first and second brightest galaxies in the cluster, and a stacked X-ray image of these 13 groups, suggests that these are young systems still in the process of forming.

     
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    Distyly is an intriguing floral adaptation that increases pollen transfer precision and restricts inbreeding. It has been a model system in evolutionary biology since Darwin. Although theS‐locus determines the long‐ and short‐styled morphs, the genes were unknown inTurnera. We have now identified these genes.

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    Thes‐haplotype possessed 21 genes collinear with a region of chromosome 7 of grape. TheS‐haplotype possessed three additional genes and two inversions.TsSPH1was expressed in filaments and anthers,TsYUC6in anthers andTsBAHDin pistils. Long‐homostyle mutants did not possessTsBAHDand a short‐homostyle mutant did not expressTsSPH1.

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