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Multiple biological and behavioral systems work in coordination to shape development (Hostinar & Gunnar, 2013), yet coherence, or cross-correlation, between psychophysiological systems underlying behavioral dysregulation and the development of anxiety disorders in early childhood remains unclear. Both the error-related negativity (ERN), indexing cognitive control, and Respiratory Sinus Arrhythmia (RSA) suppression, indexing parasympathetic regulation, have shown independent associations with developmental risk for anxiety-related disorders (Beauchaine et al., 2007; Moser, 2017), and both regulatory systems seem to interact through similar neural mechanisms (e.g., anterior cingulate cortex) as children mature. Therefore, the current study tested the moderating role of temperamental fear (context-appropriate, context-inappropriate) when predicting coherence between ERN and intra-individual RSA suppression during a Go-no-Go (GNG) task in 3-year-old children (N=119; Mage=3.59, SD=0.15). First, to establish if a relation between behavioral task performance and ERN-RSA coherence exists, we tested GNG-errors as a moderator. When GNG-errors were high, less RSA suppression predicted larger ERN (hereafter “negative systemic coherence”; B = -8.458, SE(B) = 2.667, 95% CI [-12.846, -4.070], p = .002). We then tested the moderating role of context-appropriate and context-inappropriate fear when predicting ERN-RSA coherence. Less RSA suppression predicted larger ERN (i.e., negative systemic coherence) when context-appropriate fear was low (B = -10.47, SE(B) = 3.24, 95% CI [-15.80, -5.13], p < .01) but context-inappropriate fear was high (B = -11.88, SE(B) = 4.16, 95% CI [-1.22, -0.37], p < .01). To better characterize the degree to which ERN-RSA coherence may denote risk for anxiety problems, we tested whether age 5 Generalized Anxiety Disorder (GAD) symptoms (Mage=5.52, SD=0.12) moderated the same age 3 relations. When levels of GAD symptoms were high, children showed more negative systemic coherence (i.e., less suppression coupled with larger ERN) at age 3 (B = -17.81, SE(B) = 5.00, 95% CI [-26.04, -9.58], p < .01). When GAD symptoms were low, children showed more positive systemic coherence (i.e., more suppression coupled with larger ERN; B = 21.432, SE(B) = 7.781, 95% CI [8.633, 34.232], p = .006). Finally, to understand whether ERN-RSA coherence may denote a broader risk for behavioral problems, we tested neuroendocrine (i.e., cortisol) reactivity at age 5 as a moderator. When cortisol reactivity was high, children showed more positive systemic coherence (i.e., more suppression coupled with larger ERN; B = 11.472, SE(B) = 4.033, 95% CI [4.837, 18.107], p = .004). When cortisol reactivity was low, children showed more negative systemic coherence (i.e., less suppression coupled with larger ERN; B = -22.287, SE(B) = 4.136, 95% CI [-29.090, -15.483], p < .001). Overall, results suggest negative ERN-RSA coherence during GNG is associated with reduced behavioral performance and increased risk-related behaviors (i.e., context-inappropriate fear) at age 3. Additionally, negative ERN-RSA coherence at age 3 was associated with blunted neuroendocrine reactivity, a potential chronic stress response, and early-emerging GAD symptoms by age 5. These results suggest a novel relation between cortical and parasympathetic regulatory systems in early childhood which may further characterize developmental trajectories for anxiety-related disorders and enduring behavioral dysregulation.