Gene order and genetic distance of 13 loci spanning murine chromosome 15

Hameister, Horst; Schulz, Wolfgang A.; Meyer, Jobst; Thoma, Stefan; Adolph, Sabine; Gaa, Andreas; Deimling, Otto von

doi:10.1016/s0888-7543(05)80235-6

Cited by 4 publications

(2 citation statements)

References 33 publications

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“…The eGFP transgene was genotyped by PCR with the forward primer GFP-F1 (5'-CTGGTCGAGCTGGACGGCGACG-3') and reverse primer GFP-R1 (5'-CACGAACTCCAGCAG-GACCATG-3'). The scid and IL2Rg null mutations were genotyped using a previously described PCR method [2,3]. Three to six microsatellite markers were selected from each chromosome, including the X-chromosome.…”

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“…One major problem is that a larger gap might not be able to detect a double crossing-over occurring in meiosis. Hameister et al examined the frequency of double crossing-over in a 55.4-cM region between chromosome 15A2 and 15F2-3 in 151 mice and found only one animal with a double crossing-over [2]. In reality, double crossing-over does not occur at a high frequency, even in a larger gap extending over 50 cM.…”

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Establishing EGFP Congenic Mice in a NOD/Shi-scid IL2Rgnull (NOG) Genetic Background Using a Marker-Assisted Selection Protocol (MASP)

et al. 2008

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Establishing EGFP Congenic Mice in a NOD/Shi-scid IL2Rgnull (NOG) Genetic Background Using a Marker-Assisted Selection Protocol (MASP)

et al. 2008

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Central Nervous System

Sergi

2020

Pathology of Childhood and Adolescence

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The vesicular forebrain (pseudo-aprosencephaly): a missing link in the teratogenetic spectrum of the defective brain anlage and its discrimination from aprosencephaly

Sergi

Schmitt

2000

Acta Neuropathol

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Two cases out of a sample of 41 fetuses and infants with prosencephalic malformation, observed at the Institute of Pathology and Department of Neuropathology of the University of Heidelberg, are described here in detail. These cases presented grossly with microcephaly and missing forebrain, appearing to be cases of aprosencephaly. However, in one of these cases glio-mesenchymal membranes with an ependymal outline, consistent with the microscopic appearance of the dorsal sac membrane in holoprosencephaly and obviously representing remnants of a collapsed primitive prosencephalic vesicle, could be demonstrated. In the other case only hindbrain structures, with the exception of the cerebellum, were present without any demonstrable remnants of a prosencephalon. We propose that the microscopic specification of a primitive prosencephalic vesicle in the first case and similar cases does not justify the diagnosis of atelencephaly/aprosencephaly because the prosencephalon was not really missing (pseudo-aprosencephaly). The prosencephalic anlage had been formed but remained vesicular without further differentiation of a holospheric brain mantle as in common holoprosencephaly ('vesicular forebrain'). We believe that pseudo-aprosencephaly represents the most primitive form of holoprosencephaly, in which the forebrain remains as a complete sac, linking classical holoprosencephaly with 'true' aprosencephaly, i.e., defective prosencephalic anlage due to developmental arrest. The 'vesicular forebrain' allows one to extend the classification of Probst by an additional category which might be termed complete sac category, intercalated between the dorsal sac category and 'true' atelencephaly/aprosencephaly.

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Gene order and genetic distance of 13 loci spanning murine chromosome 15

Cited by 4 publications

References 33 publications

Establishing EGFP Congenic Mice in a NOD/Shi-scid IL2Rgnull (NOG) Genetic Background Using a Marker-Assisted Selection Protocol (MASP)

Establishing EGFP Congenic Mice in a NOD/Shi-scid IL2Rgnull (NOG) Genetic Background Using a Marker-Assisted Selection Protocol (MASP)

Central Nervous System

The vesicular forebrain (pseudo-aprosencephaly): a missing link in the teratogenetic spectrum of the defective brain anlage and its discrimination from aprosencephaly

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