Table 5.

Ps is required for increased inclusion of exon L

Genotype/drug	DmNav	J	I	A	B	C	D	E	F	H	K	L	# Clones	%
sda+/−, ps+/−	31		I		B		D		F			L	20	25.6
	30		I	A	B		D		F			L	13	16.7
	33		I	A	B		D					L	11	14.1
	29		I		B		D	E				L	6	7.7
	43		I		B		D					L	6	7.7
	26		I		B		D		F		K		5	6.4
	34		I		B		D		F	H		L	3	3.8
	58		I	A	B		D				K		3	3.8
	84		I	A	B		D	E					3	3.8
	41		I	A	B		D	E				L	2	2.6
	50		I	A	B		D		F				2	2.6
	63		I				D		F			L	2	2.6
	65		I		B		D		F				2	2.6
ps+/− + PTx	30		I	A	B		D		F			L	27	29.0
	31		I		B		D		F			L	26	28.0
	33		I	A	B		D					L	15	16.1
	32		I	A	B		D		F	H		L	8	8.6
	43		I		B		D					L	5	5.4
	26		I		B		D		F		K		4	4.3
	47		I	A	B		D		F	H	K		2	2.2
	54		I	A	B		D		F		K		2	2.2
	55		I	A	B		D			H		L	2	2.2
	60		I		B		D				K		2	2.2

Loss of one copy of ps rescues the increased inclusion of exon L normally seen in whole CNS in the sda mutation (100 vs 88.9%; compared with 87.8% in WT controls, p ≤ 0.05; see Table 4). Similarly, the effect of feeding PTx to WT larvae is also rescued by loss of one copy of ps (100 vs 89.0%, p ≤ 0.05). Nomenclature of DmNa_v splice variants has been described previously (Lin et al., 2009). Only those splice variants present in two or more copies are shown isolated from 100 (comprising duplicates of 50 and 50) and 113 (comprising duplicates of 52 and 61) clones, respectively. DmNa_vs shown in bold (i.e., 50, 65, and 84) are nonfunctional. These clones are shown for reference only and have not been used for determination of frequency of inclusion for exons K and L. The letters J–L denote alternative exons in DmNa_v, and the presence of the letter denotes inclusion in the transcript (for details, see Lin et al., 2009).