Zinc-finger transcriptional repressor (PubMed:24550111, PubMed:24618901, PubMed:28245922). In larval brain, involved in the maintenance of cell fate of intermediate neural progenitors (INPs) that derive from type II neuroblasts (PubMed:20152183, PubMed:24618901, PubMed:27151950, PubMed:27510969, PubMed:28245922, PubMed:28899667). Restricts INP developmental potential and dedifferentiation by interacting with HDAC3 and the chromatin remodeling Brahma-associated protein (BAP) complex (PubMed:24618901, PubMed:24550111, PubMed:27151950, PubMed:28899667, PubMed:28245922). Restricts INP proliferation by regulating neuroblast specific factors such as prospero, pnt and grh, and by antagonizing the function of self-renewal factors, such as klu, dpn and E(spl)mgamma-HLH (PubMed:20152183, PubMed:24550111, PubMed:28899667). In the optic lobe, essential for coordinating the innervation/ targeting of the L3 and R8 axons to the M3 layer of the medulla (PubMed:29513217). Early in medulla development, functions in parallel to CadN and Sema1a pathways to promote targeting of the L3 growth cones to the proximal domain of the outer medulla possibly by controlling the expression of various cell surface genes such as dpr1 and dpr17 which function in L3 growth cone targeting (PubMed:29513217). Then once L3 growth cones segregate into the developing M3 layer, it activates the expression of netrins NetA and NetB which act locally to promote the attachment of R8 growth cones within the M3 layer (PubMed:29513217). Found in a probable chromatin remodeling Brahma-associated proteins (BAP) complex composed of at least brm, Bap60, Snr1 and erm. Within the complex, interacts (via N-terminus) with Bap60 and HDAC3. Expressed in immature intermediate neural progenitors (INP) and type II neuroblasts in larval brains (at protein level) (PubMed:24550111, PubMed:27151950, PubMed:27510969, PubMed:28245922). Expressed in lamina L3 neurons from early pupal to adult stages, but is absent in late third instar larvae when lamina neurons begin to differentiate (at protein level) (PubMed:29513217). Expressed in the developing embryonic brain from stage 4 (PubMed:18621688). The second, third and fourth zinc finger domains are necessary for repressing gene transcription. Results in abnormal expansion of type II neuroblasts and in ectopic expression of pnt and grh (PubMed:28245922, PubMed:20152183). Simultaneous RNAi-mediated knockdown of N partially restores normal neuroblast numbers and prevents loss of pnt expression (PubMed:27151950). Simultaneous RNAi-mediated knockdown of erm with either HDAC3 or members of the Brm-associated protein (BAP) chromatin-remodeling complex brm and Snr1 further increases the number of type II neuroblasts compared with the single knockdown (PubMed:24618901). Simultaneous RNAi-mediated knockdown of both erm and the ETS protein pnt restores normal neuroblast numbers (PubMed:28899667). RNAi-mediated knockdown in lamina neurons and their precursor cells, results in defective targeting of R8 neurons, with 45% of them terminating in medulla layers other than the correct M3 layer (PubMed:29513217). RNAi-mediated knockdown in L3 neurons, reduces expression of NetB in L3 neurons, L3 somas and the developing M3 layer (PubMed:29513217). Belongs to the krueppel C2H2-type zinc-finger protein family.