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. 2001 Jan 15;21(2):513–526. doi: 10.1523/JNEUROSCI.21-02-00513.2001

Table 3.

Counts of FRUM-expressing cells in the pupal CNS of fru mutants

Neuronal cluster WT fru2/fru2 fru3/fru3 fru4/fru4 frusat/frusat fru1/fru3 fru1/fru4 fru1/fruw24
Anterior brain
fru-aSP1 16  ± 1 16  ± 1 (4) 0  (10) 0  (4) 0  (4) 7  ± 1 (5) 6  ± 1 (3) 0 (4)
fru-aSP2 57  ± 2 44  ± 3 (5) 0  (10) 0  (4) 0  (4) 19  ± 1 (5) 28  ± 1 (3) 16  ± 1 (4)
fru-aSP3 40  ± 3 36  ± 2 (4) 0  (10) 0  (4) 5  ± 1 (3) 24  ± 3 (5) 38  ± 1 (3) 6  ± 2 (3)
fru-Lv 17  ± 1 18  ± 1 (4) 0  (10) 0  (4) 5  ± 2 (2) 15  ± 1 (5) 20  ± 4 (3) 9  ± 1 (4)
fru-mAL 29  ± 1 22  ± 1 (4) 0  (10) 0  (4) 0  (4) 7  ± 1 (5) 10  ± 2 (3) 1  ± 1 (3)
fru-AL 54  ± 3 46  ± 1 (5) 0  (10) 0  (4) 9  ± 2 (4) 46  ± 4 (7) 50  ± 2 (4) 29  ± 6 (2)
fru-mcAL 30  ± 1 25  ± 4 (2) 0  (10) 0  (4) 0  (4) 32  ± 2 (5) 33  ± 2 (4) 27  ± 2 (3)
Spanning portions of both anterior and posterior brain
fru-SG 12  ± 1 16  ± 2 (4) 0  (10) 0  (4) 0  (4) 7  ± 1 (3) 9  ± 2 (4) 7  ± 4 (2)
fru-M 164  ± 8 N.A. 0  (10) 0  (4) 0  (4) N.A. N.A. N.A.
fru-Ld 50  ± 4 N.A. 0  (10) 0  (4) 0  (4) N.A. N.A. N.A.
fru-Lo 34  ± 1 N.A. 0  (10) 0  (4) 0  (4) N.A. N.A. N.A.
Posterior brain
fru-pSP1 7  ± 1 7  ± 1 (2) 0  (10) 0  (4) 0  (4) 6  ± 1 (3) 7  ± 1 (4) 4  ± 1 (3)
fru-pSP2 16  ± 1 16  ± 2 (4) 0  (10) 4  ± 1 (4) 7  ± 1 (3) 15  ± 2 (3) 14  ± 1 (4) 6  ± 2 (2)
fru-P 73  ± 4 62  ± 1 (4) 0  (10) 5  ± 1 (4) 20  ± 4 (4) 87  ± 13 (3) 76  ± 4 (4) 59  ± 6 (2)
fru-pL 12  ± 2 11  ± 2 (4) 0  (10) 0  (4) 0  (4) 11  ± 2 (3) 12  ± 2 (5) 14  ± 1 (2)
Thoracic ganglia
fru-Pr 21  ± 1 17  ± 1 (4) 0  (10) 0  (4) 0  (4) 15  ± 1 (4) 14  ± 2 (5) 9  ± 2 (2)
fru-PrMs 83  ± 1 71  ± 1 (4) 0  (10) 0  (4) 10  ± 1 (4) 49  ± 3 (3) 57  ± 3 (3) 31  ± 2 (2)
fru-MsMt 52  ± 4 35  ± 2 (4) 0  (10) 0  (4) 4  ± 1 (4) 25  ± 3 (3) 29  ± 2 (3) 27  ± 9 (2)
fru-MtAb 14  ± 1 8  ± 2 (4) 0  (10) 0  (4) 0  (4) 10  ± 1 (3) 11  ± 1 (3) 14  ± 2 (3)
Abdominal ganglion
fru-Ab 91  ± 3 83  ± 2 (4) 0  (10) 0  (4) 8  ± 1 (4) 44  ± 2 (3) 49  ± 5 (3) 24  ± 3 (3)

Immunostaining was mediated by application of anti-FRUM to the CNS of 2-d-old pupal males of various homozygous or heterozygous fru types (including homozygousfru+ = wild-type = WT). Allfru variants indicated are mutant alleles exceptw24, which designates a fru-locus deletion. Numerical data from the fru1 mutant are not included, because there are too many weakly stained, ectopically located cells to count them accurately; and the more intensely labeled cells in the various ganglia of this mutant (putative subsets of the WT patterns) could not necessarily be distinguished on a cell-by-cell basis from those with “weak” signals (Figs. 3-5). Numbers (mean ± SEM) of signal-containing neurons were counted within a given neuronal group for one side of the brain or the VNC (see below);n values for these hemi-ganglia are in parentheses. The neuronal groupings (leftmost column) were classified as in Lee et al. (2000), and in fact the numbers of FRUM cells within the various WT neuronal clusters (leftmost data column) are from that report (although in it, results of the cell counts were quoted as mean ± range). The complete absence of staining within a given CNS region is indicated by a “zero” count. For most specimens, counts of immunostained neurons were made for the cluster in question within the left or (bilaterally symmetrical) right side of the brain or ventral nerve cord; when both sides of a CNS were used, the left and right counts were treated independently. Values in boldindicate that there was at least an approximately twofold difference between the mean mutant value compared with that of WT (bold not used for the obvious “zero” mutant cases). Despite the appearance (under the microscope) of signal-containing neurons in brain clustersfru-M, fru-Ld, and fru-Lo in three of the mutant types, cell counts were not performed because of extremely low staining levels in these regions for pupae of these genotypes (thus, N.A., data not available).