At four o’clock in the morning, in the street in front of our home, I nearly lose it. Our three-week old has been crying for ten hours. I’ve wrestled her into a sling and am jumping up and down under a streetlight, singing “Amazing Grace” in agitated bursts.

Things have taken a turn for the worse. Earlier in the day when I lifted the baby up to my face, eyeball to eyeball, she jerked her head away and cried harder. The infant has been rocked and bounced, shushed and swaddled – with increasing force and desperation. It occurs to me that maybe I should ignore her for a spell. I could lay her down on the dewy grass, let her scream at the stars and the moon, while I drop my head in my hands and weep. How sweet the sound.

If there’s a mommy gene, I don’t have it.

Mommy genes! The idea started about fifteen years ago when a doctoral student named Jennifer Brown and her colleagues at Harvard Medical School noticed something wrong with their mice experiment. Pups were dying. Whole litters, in fact, were wiped out just a day or two after birth. This was strange, because the babies were healthy and so were the mothers. One glance at the mouse cage solved the mystery. Pups were scattered everywhere, shivering and starving, while the mothers nonchalantly went about their business. Normal mother mice round up their brood and feed and lick them. But these dams didn’t give a damn. They acted oblivious to their babies’ frantic squeaks.

The mother mice were specially bred to lack a gene called fosB. Brown and her colleagues had no idea that knocking out fosB would make mice into deadbeat moms, but it apparently does. It turns out that the gene, when activated, creates a protein that turns on other genes and is partly responsible for the function of neurons in the hypothalamus, a region of the brain that controls emotional behavior — including nurture. If you’re a murine mother, just being around your babies usually triggers the fosB gene to express itself. Because mother mice lacking a working copy of the gene are not motherly, fosB hit the headlines as the first “mommy gene.”

Several years later researchers found that genes called Peg 1/Mest and Peg3 also have an effect on the motherliness of mice. When scientists disabled these genes the result was similar the FosB experiment: cold-hearted mothers, empty-bellied pups. Both these genes influence how oxytocin, the “love hormone” behind caressing and nursing and other mothering behavior, is processed in the brain. When oxytocin doesn’t get to where it needs to go, the result is less nurture, more neglect. (Interestingly, in mice and humans, only the Peg1/Mest and Peg3 genes are imprinted and only the one inherited from the father is active. This means an afflicted mouse can blame her lack of mothering instinct on her dads. An attentive one can give him credit. )

“More Mommy genes!” the headlines raved. Mice and humans share many of the same genes, so these genes may influence women’s nurturing instincts, too. Perhaps we can test every wannabe mom to see if she has working copies of FosB, Peg1/ Mest, and Peg3. Then we’ll know who can soothe babies into submission and who thinks it’s a good idea to leave them to cry under the stars. Perhaps we can use genetic engineering to make us supermoms. No new parent would feel exasperated and hopeless again. Let’s make sure everyone has warm fuzzy mommy genes.

The scientists doing this research never claimed they found mommy genes. That sort of bravado would be embarrassing. Humans are obviously more complex than mice, and our behavior is more nuanced.

To say a gene makes a woman a good mother is a little like saying the carburetor is what makes a plane fly. Sure, the plane wouldn’t get off the ground without the device to blend air and fuel. But to credit the carburetor for flight? What about the wings, the pilot, the fuel? Or even the screws and the steel? And what about air around the plane, and the molecules in it? We can’t give all the credit (or blame) to one widget.

The same goes for “mommy genes.” Sure, genes influence how proteins are transcribed and neurons fire and signals are dispatched and hormones are received and processed, and so on. Every part of this infrastructure supports our nurturing behavior. We may be especially deficient if particular genes are defective or if they malfunction. There’s no doubt that researching these genes gives us valuable information about our nurturing behavior. But it’s likely that any one gene is just a widget in what makes us fly.

What’s a good mommy, anyway? That’s a debate beyond the realm of science. It’s slippery. When my newborn finally falls asleep in my arms, angelically, clutching my pinky, I feel like a good mommy again. It doesn’t require mommy genes.

It takes amazing grace.