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. 2019 Jan 1;8:e42078. doi: 10.7554/eLife.42078

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© 2019, Pereira et al

This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.

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Figure 5. — (A) The neurotransmitter switch is blocked in three newly generated lin-29 mutants. In adult control animals, the fosmid-based cholinergic reporters unc-17/VACHT (otIs576) and cho-1/CHT (otIs544) are expressed in AIM neurons of adult males but not hermaphrodites while the eat-4/VGLUT (otIs518) glutamatergic reporter is expressed in AIM neurons of adult hermaphrodites but not males. The AIM neurotransmitter switch is blocked in a newly generated lin-29a/b(xe37) null allele and in two lin-29a-specific mutants (xe38 and xe40). In these lin-29 mutant males, AIM fails to turn on cholinergic markers unc-17/VACHT (top panels) and cho-1/CHT (bottom panels) and expresses a pan neuronal maker rab-3::rfp (top panels) and the glutamatergic marker eat-4/VGLUT (bottom panels). A pan-neuronal rab-3::rfp (otIs355) reporter was used to label all neurons in the top panels. (B) AIM-specific LIN-29A expression is sufficient to cell-autonomously rescue the neurotransmitter switch in males and induce it in young larvae and the opposite sex. LIN-29A expression was driven under an AIM-specific promoter in lin-29a mutant animals: LIN-29A was expressed in lin-29a(xe38) (otEx7316 and otEx7317) and in lin-29a(xe40) (otEx7318 and otEx7319). Expression of cholinergic gene reporter unc-17/VACHT (otIs576) was examined to assay rescue and ectopic induction of the AIM neurotransmitter switch (n = 15).