using ion channel opener/blocker drugs, as well as dominant ion channel misexpression, in a range of model species, has shown that bioelectricity, specifically, voltage gradients instruct not only stem cell behavior but also large-scale patterning. patterning cues are often mediated by spatial gradients of cell resting potentials, or vmem, which can be transduced into second messenger cascades and transcriptional changes by a handful of known mechanisms. these potentials are set by the function of ion channels and pumps, and shaped by gap junctional connections which establish developmental compartments (isopotential cell fields). because both gap junctions and ion channels are themselves voltage-sensitive, cell groups implement electric circuits with rich feedback capabilities. the outputs of developmental bioelectric dynamics in vivo represent large-scale patterning decisions such as the number of heads in planaria, the shape of the face in frog development, and the size of tails in zebrafish. experimental modulation of endogenous bioelectric prepatterns have enabled converting body regions (such as the gut) to a complete eye, inducing regeneration of appendages such as tadpole tails at non-regenerative contexts, and conversion of flatworm head shapes and contents to patterns appropriate to other species of flatworms, despite a normal genome. recent work has shown the use of physiological modeling environments for identifying predictive interventions to target bioelectric states for repair of embryonic brain defects under a range of genetic and pharmacologically-induced teratologies. future research life is ultimately an electrochemical enterprise; research in this field is progressing along several frontiers. first is the reductive program of understanding how bioelectric signals are produced, how voltage changes in the cell membrane are able to regulate cell behavior, and what the genetic and epigenetic downstream targets of bioelectric signals are. a few mechanisms that transduce bioelectric change into alterations of gene expression are already known, including the bioelectric control of movement of small second-messenger molecules through cells, including serotonin and butyrate, voltage sensitive phosphatases, among others. also known are numerous gene targets of voltage signaling, such as notch, bmp, fgf, and hif-1α. thus, the proximal mechanisms of bioelectric signaling within single cells are becoming well-understood, and advances in optogenetics and magnetogenetics continue to facilitate this research program. more challenging however is the integrative program of understanding how specific patterns of bioelectric dynamics help control the algorithms that accomplish large-scale pattern regulation (regeneration and development of complex anatomy). the incorporation of bioelectrics with chemical signaling in the emerging field of probing cell sensory perception and decision-making is an important frontier for future work. bioelectric modulation has shown control over complex morphogenesis and remodeling, not merely setting individual cell identity. moreover, a number of the key results in this field have shown that bioelectric circuits are non-local – regions of the body make decisions based on bioelectric events at a considerable distance. such non-cell-autonomous events suggest distributed network models of bioelectric control; new computational and conceptual paradigms may need to be developed to understand spatial information processing in bioelectrically-active tissues. it has been suggested that results from the fields of primitive cognition and unconventional computation are relevant to the program of cracking the bioelectric code. finally, efforts in biomedicine and bioengineering are developing applications such as wearable bioreactors for delivering voltage-modifying reagents to wound sites, and ion channel-modifying drugs (a kind of electroceutical) for repair of birth defects and regenerative repair. synthetic biologists are likewise starting to incorporate bioelectric circuits into hybrid constructs. table 1: ion channels and pumps implicated in patterning protein morphogenetic role or lof (loss of function) phenotype species reference trh1 k+ transporter root hair patterning arabidopsis kir2.1potassium channel wing patterning drosophila kir7.1 k+ channel craniofacial patterning, lung development mus musculus nhe2 na+/h+ exchanger epithelial patterning drosophila v-atpase proton pump wing hair patterning, pigmentation and brain patterning, craniofacial patterning drosophila, oryzias latipes, homo sapiens hcn1, kv3.1 k+ channels forebrain patterning mus musculus kcnc1 k+ channel growth deficits mus musculus twik-1 k+ channel (kcnk1) cardiac (atrial) size mus musculus kcnj6 k+channel keppen-lubinsky syndrome – craniofacial and brain homo sapiens kcnh1 (heag1) k+ channel and atp6v1b2 v-atpase proton pump zimmermman-laband and temple-baraitser syndrome – craniofacial and brain defects, dysplasia/aplasia of nails of thumb and great toe. homo sapiens glra4 chloride channel craniofacial anomalies homo sapiens kcnj8 k+ cantu syndrome – face, heart, skeleton, brain defects homo sapiens nalcn (na+ leak channel) freeman-sheldon syndrome – limbs, face, brain homo sapiens cftr chloride channel bilateral absence of vas deferens homo sapiens kcnc1 head/face dysmorphias homo sapiens kcnk9, task3 k+ channels birk-barel dysmorphism syndrome – craniofacial defects, brain (cortical patterning) defects homo sapiens kir6.2 k+ channel craniofacial defects homo sapiens kcnq1 k+ channel (via epigenetic regulation) hypertrophy of tongue, liver, spleen, pancreas, kidneys, adrenals, genitalia – beckwith-wiedemann syndrome; craniofacial and limb defects, early development homo sapiens, mus musculus, drosophila kcnq1 k+ channel jervell and lange-nielsen syndrome - inner ear and limb homo sapiens, mus musculus kir2.1 k+ channel (kncj2) andersen-tawil syndrome – craniofacial, limb, ribs homo sapiens, mus musculus gaba-a receptor (chloride channel) angelman syndrome - craniofacial (e.g., cleft palate) and hand patterning homo sapiens, mus musculus tmem16a chloride channel tracheal morphogenesis mus musculus girk2 k+ channel cerebellar development defects mus musculus kcnh2 k+ channel cardiac, craniofacial patterning defects mus musculus kcnq1 k+ channel abnormalities of rectum, pancreas, and stomach mus musculus nav1.2 muscle and nerve repair defects xenopus kir6.1 k+ channel eye patterning defects xenopus v-atpase ion pump left-right asymmetry defects, muscle and nerve repair xenopus, gallus gallus domesticus, danio rerio h,k-atpase ion pump left-right asymmetry defects xenopus, echinoidea kir7.1 k+ channel melanosome development defects danio rerio kv channels fin size regulation, heart size regulation danio rerio, mus musculus nav 1.5, na+/k+-atpase cardiac morphogenesis danio rerio kcnc3 dominant mutations cause cerebellar displasia in humans, and wing venation and eye defects in drosophila. homo sapiens, drosophila table 2: gap junctions implicated in patterning gap junction protein morphogenetic role or lof phenotype species