++ +Almost all animals are young adults between 60 and 90 days of age (Table 1, minimum age is 48 and maximum age is 118 days). We measured expression in conventional inbred strains, BXD recombinant inbred (RI) strains, and reciprocal F1s between C57BL/6J and DBA/2J.
+ +BXD strains: + +++
+- The first 32 of these strains are from the Taylor series of BXD strains generated at the Jackson Laboratory by Benjamin A. Taylor. BXD1 through BXD32 were started in the late 1970s, whereas BXD33 through 42 were started in the 1990s.
+- In 2004, BXD24/TyJ developed a spontaneous mutation, rd16 which resulted in retinal degeneration and was renamed BXD24b/TyJ (BXD24 in this database). The strain, BXD24a, was cryo-recovered in 2004 from 1988 embryo stocks (F80) and does not exhibit retinal degeneration. In 2009, BXD24b was renamed BXD24/TyJ-Cep290rd16/J by JAX Labs to reflect the discovery of the genetic basis of the mutation. At the same time BXD24a was then referred to just as BXD24/TyJ by Jax Labs, but still called BXD24a in this dataset.
+- The other 36 BXD strains (BXD43 and higher) were bred by Lu Lu, Jeremy Peirce, Lee M. Silver, and Robert W. Williams starting in 1997 using B6D2 generation 10 advanced intercross progeny. This modified breeding protocol doubles the number of recombinations per BXD strain and improves mapping resolution (Peirce et al. 2004). All of the Taylor series of BXD strains and many of the new BXD strains are available from the Jackson Laboratory. All of the new BXD strains (BXD43 and higher) are also available directly from Lu Lu and colleagues at the University of Tennessee Health Science Center in Memphis, TN, USA. BXD24/TyJ is now known as BXD24b/TyJ and has nearly complete retinal degeneration. BXD24a/TyJ, a 1988 F80 inbred stock that has been rederived from cryogenic storage, does not have retinal degeneration (stock number 005243) and is an ideal coisogenic control, but is not included in the HEI data set.
+
What Makes the G2 HEI Retina Database different from the HEI Retina Database Examination of Gfap expression across all of the strains in the HEI Retinal Dataset, reveals that some strains express very high levels of Gfap relative to others. For example, BXD24 expresses Gfap at a 9-fold higher level, than BXD22. It has been established that BXD24 acquired a mutation in Cep290 that results in early onset photoreceptor degeneration (Chang et al., 2006). This degeneration results in reactive gliosis throughout the retina. In addition to BXD24, other BXD strains expressed very high levels of Gfap including: BXD32, BXD49, BXD70, BXD83 and BXD89. For the G2 dataset all of these strains with potential reactive gliosis were removed from the dataset.
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