5 research outputs found
The DEEP2 Galaxy Redshift Survey: Design, Observations, Data Reduction, and Redshifts
We describe the design and data sample from the DEEP2 Galaxy Redshift Survey,
the densest and largest precision-redshift survey of galaxies at z ~ 1
completed to date. The survey has conducted a comprehensive census of massive
galaxies, their properties, environments, and large-scale structure down to
absolute magnitude M_B = -20 at z ~ 1 via ~90 nights of observation on the
DEIMOS spectrograph at Keck Observatory. DEEP2 covers an area of 2.8 deg^2
divided into four separate fields, observed to a limiting apparent magnitude of
R_AB=24.1. Objects with z < 0.7 are rejected based on BRI photometry in three
of the four DEEP2 fields, allowing galaxies with z > 0.7 to be targeted ~2.5
times more efficiently than in a purely magnitude-limited sample. Approximately
sixty percent of eligible targets are chosen for spectroscopy, yielding nearly
53,000 spectra and more than 38,000 reliable redshift measurements. Most of the
targets which fail to yield secure redshifts are blue objects that lie beyond z
~ 1.45. The DEIMOS 1200-line/mm grating used for the survey delivers high
spectral resolution (R~6000), accurate and secure redshifts, and unique
internal kinematic information. Extensive ancillary data are available in the
DEEP2 fields, particularly in the Extended Groth Strip, which has evolved into
one of the richest multiwavelength regions on the sky. DEEP2 surpasses other
deep precision-redshift surveys at z ~ 1 in terms of galaxy numbers, redshift
accuracy, sample number density, and amount of spectral information. We also
provide an overview of the scientific highlights of the DEEP2 survey thus far.
This paper is intended as a handbook for users of the DEEP2 Data Release 4,
which includes all DEEP2 spectra and redshifts, as well as for the
publicly-available DEEP2 DEIMOS data reduction pipelines. [Abridged]Comment: submitted to ApJS; data products available for download at
http://deep.berkeley.edu/DR4
Female Infertility and Disrupted Angiogenesis Are Actions of Specific Follistatin Isoforms
The circulating and tissue-bound forms of follistatin (FST315 and FST288, respectively) modulate the actions of activins. FST knockout (KO/null) mice, lacking both isoforms, die perinatally with defects in lung, skin, and the musculoskeletal system. Using constructs of the human FST gene engineered to enable expression of each isoform under the control of natural regulatory elements, transgenic mouse lines were created and crossed with FST null mice to attempt to rescue the neonatal lethality. FST288 expression alone did not rescue the neonatal lethality, but mice expressing FST315 on the KO background survived to adulthood with normal lung and skin morphology and partial reversal of the musculoskeletal defects noted in FST KO mice. The FST315 rescue mice displayed a short period of neonatal growth retardation, impaired tail growth, and female infertility. The latter may be due to failure of corpus luteum formation, a decline in the ovarian follicular population, and an augmented uterine inflammatory response to mating. Failure of corpus luteum formation and impaired tail growth indicate abnormal vascularization and suggest that FST288 is required for the promotion of angiogenesis. The augmented uterine inflammatory response may result from the failure of FST315 to modulate the proinflammatory actions of activin A in the uterus or may result from the altered steroid milieu associated with the ovarian abnormalities. Although we cannot definitively conclude that the remaining defects are due to the absence of a particular isoform or due to variable expression of each, these models have demonstrated novel physiological processes that are influenced by FST